The Politics of Causation
The Nature of a New Threat
The Discovery of a "Gay Disease" (1981-1982)
When a puzzling new medical syndrome was first reported to be afflicting—and killing—young gay men in certain cities in the United States, there was no particular reason to expect that the cause might be a previously unknown virus. Nor did the deaths immediately take on any great medical significance. Michael Gottlieb, a young immunologist at the teaching hospital of the University of California at Los Angeles, began seeing such cases in late 1980 but found that he couldn't spark the interest of the New England Journal of Medicine , the most prestigious medical journal in the country, later to publish hundreds of articles on AIDS. In early 1981 the New England Journal 's editor instead referred Gottlieb to the U.S. Centers for Disease Control (CDC), the federal agency in Atlanta, Georgia, responsible for tracking diseases and controlling their spread.
The CDC's first report, published in its Morbidity and Mortality Weekly Report in June 1981, noted only that five young men in Los Angeles, "all active homosexuals," had been treated over the course of the past year for Pneumocystis carinii pneumonia (PCP). Two of the men had died. The microorganism that causes PCP is ubiquitous but is normally kept easily at bay by the body's immune system; therefore cases of PCP were exceedingly rare, restricted to people who were
immunosuppressed because of medical treatment (such as chemotherapy) or who for other reasons had severely malfunctioning immune systems. The CDC report zeroed in on the question of sexuality—"the fact that these patients were all homosexual"—to put forward two tentative hypotheses: that the PCP outbreak was associated with "some aspect of a homosexual lifestyle" or with "disease acquired through sexual contac." However, "the patients did not know each other and had no known common contacts or knowledge of sexual partners who had had similar illnesses."
A few weeks later, the CDC reported twenty-six cases (twenty in New York City and six in California) of young homosexual men suffering from Kaposi's sarcoma, a rare form of cancer normally found in elderly men. At least four of the men also had cases of PCP; eight of them had died. On the basis of this report, Dr. Lawrence Altman, medical reporter for the New York Times , wrote a short article about the cases of cancer in homosexuals. Appearing deep inside the newspaper on page A-20, the article sounded what would become one of the most common themes in mainstream media coverage of the epidemic: "The reporting doctors said that most cases had involved homosexual men who have had multiple and frequent sexual encounters with different partners, as many as ten sexual encounters each night up to four times a week." Soon after, Dr. Lawrence Mass, health writer for the New York Native —the most widely read gay newspaper in New York City and one of only a few to have a national readership—also addressed the question of promiscuity. In an article about "Cancer in the Gay Community," Mass wrote: "At this time, many feel that sexual frequency with a multiplicity of partners—what some would call promiscuity—is the single overriding risk factor. …"
Mass's article also explored a range of possible explanations for what he called (in quotes) "the gay cancer," including "an infectious or otherwise cancerous agent," but he noted that the "current consensus of informed opinion is that multiple factors are involved in the present outbreak of Kaposi's sarcoma among gay males." He quoted Dr. Donna Mildvan, chief of infectious diseases at Beth Israel Medical Center, who reported a colleague's belief that the outbreak of illnesses "has to do with the bombardment, the clustering of a whole range of infectious diseases among these patients which may be exhausting their immunodefensive capacities." And he cited Dr. Alvin Friedman-Kien, a professor of dermatology and microbiology at New York University Medical Center, who had examined some of the Kaposi's sarcoma
patients and who had speculated about the possible role of amyl nitrite or butyl nitrite inhalants. These inhalants, street drugs that were sold legally and were popular in gay male communities at the time, were often called "poppers" because consumers would pop open the packaging to release the fumes, which were then inhaled to produce a "rush" or to intensify orgasm. Nitrites were believed to have immunosuppressive effects. On the other hand, they had been prescribed to cardiac patients for years, and no unusual cases of PCP or Kaposi's sarcoma had ever been reported in that population.
By the beginning of 1982, a series of more detailed reports in medical journals such as the New England Journal was available as a source of additional information and speculation for researchers and medical practitioners, and for translation into the media, particularly the gay press. Researchers agreed that the telltale marker of these cases of immunosuppression was a deficiency in the numbers of "helper T cells"—or in other accounts, an abnormal ratio of helper T cells to suppressor T cells—types of white blood cells involved in the body's immune response. But questions of etiology and epidemiology were considerably more confusing. For one thing, it was already apparent that the "nationwide epidemic of immunodeficiency among male homosexuals" was in fact not restricted to gay men. According to the CDC's task force on the syndrome, 8 percent of the 159 cases were among heterosexuals, one of whom was a woman. In the pages of the New England Journal , Michael Gottlieb and his coauthors, the Los Angeles clinicians who had first reported the syndrome to the CDC, described finding the same syndrome in two exclusively heterosexual men, while Henry Masur and coauthors reported eleven cases of PCP in the New York area—five injection drug users, four gay men, and two men who were both.
Nonetheless, the focus of attention in all the medical literature remained squarely on the male homosexual sufferers, as evidenced by descriptors such as Brennan and Durack's "Gay Compromise Syndrome" and Masur et al.'s more euphemistic "Community-Acquired Pneumocystis Carinii Pneumonia." All speculation about causes proceeded from the premise of the centrality of male homosexuality. In Durack's words: "What clue does the link with homosexuality provide? Homosexual men, especially those who have many partners, are more likely than the general population to contract sexually transmitted diseases. Lesbians are not, and this apparent freedom, whatever its explanation, seems to extend to Kaposi's sarcoma and opportunistic
infections." Yet the assumption that the syndrome was somehow linked with homosexuality actually did little to immediately clarify the etiology, as Durack and others realized. Noting that "male homosexuals are at increased risk for the acquisition of common viral infections" such as cytomegalovirus (CMV), hepatitis B, and Epstein-Barr virus, Durack described the "obvious problem" with the hypothesis that CMV, or any of these viruses, might be the cause: "It does not explain why this syndrome is apparently new. Homosexuality is at least as old as history, and cytomegalovirus is presumably not a new pathogen. Were the homosexual contemporaries of Plato, Michelangelo, and Oscar Wilde subject to the risk of dying from opportunistic infections?" Durack's supposition was that "some new factor," such as poppers, "may have distorted the host-parasite relatinship." Concluding with some "frank speculation," Durack put forward a model essentially identical to the one Mildvan had proposed to the Native: that "the combined effects of persistent viral infection plus an adjuvant drug cause immunosuppression in some genetically predisposed men."
This model, which was sometimes called the "immune overload" or "antigen overload" hypothesis, represented the initial medical frame for understanding the epidemic: the syndrome was essentially linked to gay men, specifically to the "excesses" of the "homosexual lifestyle." The epidemic coincided historically, Newsweek suggested in the article "Diseases That Plague Gays," "with the burgeoning of bathhouses, gay bars and bookstores in major cities where homosexual men meet." Urban gay men, enjoying "life in the fast lane," had subjected themselves to so many sexually transmitted diseases, taken so many strong treatments to fight those diseases, and done so many recreational drugs that their immune systems had ultimately given up altogether, leaving their bodies open to the onslaught of a range of opportunistic infections. As one Harvard doctor is reported to have put it informally, "overindulgence in sex and drugs" and "the New York City lifestyle" were the culprits. What distinguished gay men from CMV-infected, sexually adventurous heterosexuals, and from cardiac patients inhaling amyl nitrite, and from the many patients who took strong antibiotic or antiparisitic drugs was, these experts suggested, that only gay men (or those gay men living in the "fast lane") confronted all these risks at once.
The Politics of Lifestyle
The speculative focus on "the gay lifestyle" casts light on the very nature of epidemiological science. When a mysterious illness appears in a specific social group, it makes eminent sense to ask what distinguishes that group from others not affected, or less affected, by the illness. The difficulty is that the isolation of "difference" presupposes a common understanding of what constitutes the "background" against which this difference stands out. In this sense, epidemiology is inevitably a "normalizing" science, employing—and reinforcing—unexamined notions of normality to measure and classify deviations from the norm. Faced with a "gay disease," epidemiologists immediately fastened upon the most sensational markers of homosexual difference, trumpeting the cases of men with histories of thousands of sexual partners, while ignoring the cases, also reported by clinicians from the very beginning, of gay men who were monogamous or who engaged in relatively modest amounts of sexual experimentation.
With the advantage of hindsight, it is easy to recognize that the initial link between gay men and the new syndrome—while certainly the single most consequential aspect of the social construction of the epidemic—in fact reflected the confounding influences of what Irving Zola has called the "pathways" from doctor to patient. As Zola concluded from a more general study, it is often the case that apparent epidemiological differences in the incidence of some medical conditions actually derive from "factors of selectivity and attention which get people and their episodes into medical statistics..." There are important reasons why people do or do not seek medical help, yet, as Eliot Freidson has noted, the doctor tends to "assume that the cases he sees are no different from those he does not. And so he develops conceptions of illness that may have an inaccurate and artificial relationship to the world."
To put it simply, some people get better medical attention, which means that medical professionals "attend" to their "unique" conditions. In New York City, if not elsewhere, it appears likely that there were at least as many cases of pneumocystis pneumonia among injection drug users as among gay men at the time of he discovery of the syndrome. But gay men, some of them affluent and relatively privileged, found their way into private doctors' offices and prominent teaching hospitals—and from there into the pages of medical
journals—while drug users often sickened and died with little fanfare. Even as cases among injection drug users began to be reported, the "gay disease" frame for understanding the epidemic was already falling into place. Colloquially, the epidemic became known among some medical professionals and researchers in early 1982 as "GRID": Gay-Related Immune Deficiency.
The power of frames as organizers of experience is precisely that they work to exclude alternative ways of interpreting an experience. Because "GRID" was a "gay disease," medical practitioners and researchers sometimes resisted the idea that it might appear elsewhere, and those who proposed that the epidemic could affect other people risked being discredited within the scientific community. Randy Shilts described how, throughout 1981, "there was a reluctance [at the CDC] to believe that intravenous drug users might be wrapped into this epidemic, and the New York physicians also seemed obsessed with the gay angle.…" "He says he's not homosexual, but he must be," doctors would confide to one another. One New York pediatrician was rediculed for his contention as early as 1981 that he was seeing children suffering from the same immune dysfunction as homosexual patients.
But the differences in access to health care and the accident of the initial discovery of the syndrome among gay men are not adequate to account for the potency of this frame or the ease with which it fell into place. If gay men were perceived as plausible victims of a medical syndrome, it was in part because in the medical literature their sexualized lifestyle was already depicted as medically problematic. On one hand, epidemiologists and clinicians were genuinely surprised by the appearance of such devastating illness among "previously healthy" homosexual men. On the other hand, they were quick to make use of the existing stock of medical knowledge linking gay men with disease—specifically, the literature on sexually transmitted diseases among gay men that was published in the years just prior to, or coincident with, the onset of the epidemic. This literature, which was often cited by early medical claims-makers discussing the new epidemic of immune dysfunction, described an explosion of venereal diseases among gay men, the apparent aftermath of the "sexual revolution" and gay liberation. Concluding that homosexuality must be considered a risk factor in infectious disease, these articles stressed the need for clinicians to confront what one referred to as "homosexual hazards."
Of course, modern conceptions of gay identity have always been
partially medicalized. The very term "homosexual" dates from the nineteenth-century literature of doctors and sexologists. Gay identities have been formed, over the past one hundred years, through the dialectical interplay between an affirmative process of self-definition by homosexuals and the imposition of models by various groups of expert claims-makers. In this sense, what is ironic about the medicalization of gay male sexuality in the years just prior to the gay beginning of the epidemic is that is presupposed the successes of the gay movement, which were in part directed against an earlier medicalization (or "psychiatrization"). In opposition to a conception of homosexuality as a "mental illness," gay activists had put forward a positive conception of gay identity and the gay community. And in fact, the new medical discourse on gay men took as its starting point a particularly recent conception of the "lifestyle" of the urban gay male; this discourse marked the entry of the modern "gay community" into medical history.
While it cannot be doubted that doctors were genuinely concerned with treating the venereal diseases of gay men, the issue was framed in particular ways that influenced medical perceptions of homosexuality. First, the key phrases that were used—"homosexual hazards," "gay bowel syndrome," "homosexuality as a risk factor"—posed the problem essentially as one of identity and "lifestyle," rather thatn contraction of specific infections. (It seems far less likely that any medical journal would refer to "heterosexual hazards.") Second, the use of abstract, universalizing terms such as "the gay way of life" masked the considerable diversity of the life experiences and sexual practices of gay men; such stereotypes obscured the fact that researchers had made no attempt even to define, let alone systematically sample, the communities they characterized with rather sweeping generalizations.
Yet this was the understanding of gay male sexuality that informed medical speculation in the early days of AIDS. To be sure, the reasoning behind the immune overload hypothesis was not irrational, and the hypothesis was not absurd: after all, the epidemic was being observed mainly among gay men; many of these men did have many sexual partners; many sexually active gay men were known to contract sexually transmitted diseases, as well as use poppers and other drugs. But the strength of the resulting hypothesis depended on a long chain of implicit assumptions—that the syndrome was in essence linked to homosexuals (and the cases among heterosexuals could be explained
away); that the link to gay men meant that the epidemic was related to gay men's sexuality; that if gay men (by this view) were "promiscuous," then the illness must be a consequence of their promiscuity; and crucially, that repeated exposure to sexually transmitted pathogens (and to drugs) was actually capable of causing the immune system damage being observed. Furthermore, there was the assumption that the recent reported increases in rates of sexually transmitted disease and of drug use among gay men were indeed of sufficient magnitude to explain why the syndrome was emerging when it was.
As an initial hypothesis, immune overload was probably no more or less reasonable than many in the history of epidemiology or medical science. Nor was it ever hegemonic. For example, the first editorial on the syndrome in Lancet, the influential British medical journal, speculated on everything from "new or unrecognised environmental pollutants" to "even another infective agent"; and such conjecture continued in the medical and scientific literature throughout 1982 and 1983. where "immune overload" (or, more generally, what Murray and Payne call the "promiscuity paradigm") exerted its greatest influence was outside the world of mainstream scientific practice. Reinforced by the mainstream media and filtering out into diverse arenas, the idea of a linkage between homosexuality, promiscuity, and illness informed an emergent sensibility about the syndrome—a vision, sometimes an unarticulated perception, of the epidemic as somehow the product of "the homosexual lifestyle." At times it has been voiced as a direct accusation: as late as October 1987, North Carolina's Jesse Helms could stand on the U.S. Senate floor and proclaim that "every case of AIDS can be traced back to a homosexual act." The notion that gays brought on the AIDS epidemic—and should be held responsible for having done so—has persisted long after the decline of mainstream biomedical support for etiological arguments focusing on "the gay lifestyle."
The idea that homosexuality "causes" AIDS also indicates the tangle of meanings packed into one short word—"cause"—and the difficulties involved in carrying out a conversation about causation that cuts across a range of lay and specialist communities. As Jana Armstrong has observed, "the word `cause' is embedded in the language of public policy, the language of cell biology, the language of epidemiology. But the word does not mean the same thing in every instance of its use." Even a glance at a medical dictionary generates confusion: one such dictionary distinguishes between constitutional causes, exciting causes, immediate or precipitating causes, local causes, predisposing
causes, primary causes, proximate causes, remote causes, secondary causes, specific causes, and ultimate causes. ("Etiology" fares little better, since the definition of that term points back to the word "cause.")
Generally speaking, medical doctors were interested in finding a "primary cause"; that is, "the principal factor contributing to the production of a specific result"—in this case, the destruction of cell-mediated immune responses. But epidemiologists, in their focus on identifying risk groups, were in effect concerned significantly with "predisposing causes": "anything that renders a person more liable to a specific condition without actually producing it." Outside of the medical and scientific professions, the various usages of the word "cause" not only blurred these meanings but embedded notions of causation within a more general vocabulary of moral blame. Like cholera epidemics, which in the nineteenth-century United States were blamed on the squalid lifestyle of the poor; like gonorrhea, once regarded even by doctors as arising "from the continual irritation and excitement of the generative organs" of prostitutes; like smallpox and leprosy, which were blamed on the "unclean" practices of the U.S. Chinese population in the late nineteenth century; the genesis of the new epidemic of immune dysfunction was considered all too often with a view to assigning culpability. Partly through the power of the medical definitional process, partly through the ideological work of the opponents of gay liberation, gay men increasingly came to be equated with the emergent epidemic—it came to constitute part of their social identity.
Claiming the Epidemic
How did members of the affected communities respond to these formulations? Gay communities in the United States were both contributors to the "gay disease" frame and important critics of it. Initially, rumors of various lifestyle risks—a microbe in the water supply or the ventilation system at the most popular bathhouses, for example—spread rapidly through gay communities. Writers in the gay press showed little tendency, early on, to dispute the homosexual connection, as evidenced by the frequent use of the locution "gay cancer" (though often in quotation marks) to characterize the epidemic in 1981. This phrasing, however imprecise, effectively served as a rallying cry to alert gay men to the presence of a new danger.
Since many of the early reports in medical journals were written by
clinicians well connected to gay communities, who were treating the patients in question, many gay people—and particularly health writers such as Lawrence Mass, himself a physician—were inclined toward sympathetic views of the medical and public health authorities. Increasingly, however, many gay writers, especially in the more left-leaning publications, were openly critical of medical researchers' tendency to blame the epidemic on gay promiscuity. Much as an earlier generation of feminists had conceived of medicine as a sexist institution, these writers and activists argued that medical science was a heterosexist and sex-phobic institution that reinforced norms of sexual conformity.
Gay physicians, such as those who were members of Physicians for Human Rights, an organization of gay doctors, found themselves at the felcrum. On one hand, they were called on to introduce their professional colleagues and epidemiological investigators to many specific aspects of the "gay lifestyle," often running up against a judgmental reception within the biomedical establishment. On the other hand, they felt a sense of responsibility to warn their communities about suspected risk behaviors—but knew they would lose credibility if they were perceived to be "sex-negative" or puritanical, given that gay liberation as a political movement was so closely tied to sexual liberation as a personal ethic.
By early 1982, gay and lesbian activists had created two grassroots organizations that would prove to be pivotal in confronting the epidemic: the Gay Men's Health Crisis in New York City and, across the country, the Kaposi's Sarcoma Research and Education Foundation, later renamed the San Francisco AIDS Foundation. A testament to the high degree of political mobilization and access to resources in gay communitiess at the time, the appearance of these organizations marked simultaneous attempts to provide services to people suffering from the syndrome, relay relevant information rapidly to gay men at risk, and serve as an organized voice regarding questions of public policy.
In the early period, these organizations took no position on the question of etiology. As the Gay Men's Health Crisis advised gay New Yorkers in an open letter in mid-1982: "Unsettling though it is, no evidence exists to incriminate any activity, drug, place of residence or any other factor, conclusively, in the outbreak facing us." At the same time, simply by organizing gay communities to confront—and, in effect, claim—the epidemic, these organizations helped to solidify the popular connection between the syndrome and homosexuality (as
even the name "Gay Men's Health Crisis" implied). AIDS became a "gay disease" primarily because clinicians, epidemiologists, and reporters perceived it through that filter, but secondarily because gay communities were obliged to make it their own.
Lifestyle vs. Virus (1982–1983)
The Expansion of Risk
Sensitive to the fact that gay doctors and activists criticized the informal "GRID" designation, the CDC came up with an official name for the epidemic in May 1982 and first used the term in print in September of that year. This name was chosen specifically for its neutrality—Acquired Immunodeficiency Syndrome, or AIDS: "acquired" to distinguish it from congenital defects of the immune system; "immunodeficiency" to describe the underlying problem, the deterioration of immune system functioning (and specifically, a decline in the numbers of helper T cells, causing the body to lose most of its capacity to ward off infection); and "syndrome" to indicate that the condition was not a disease in itself, but rather was marked by the presence of some other, relatively uncommon disease or infection (like PCP or Kaposi's sarcoma), "occurring in a person with no known cause for diminished resistance to that disease." This was strictly a "surveillance" definition, for epidemiological reporting purposes: it did not imply any knowledge about what AIDS "really was." But in the absence of a lab test for a known cause, this definition at least allowed the CDC a crude measure of the scope of the problem.
The newly defined syndrome would, over the course of 1983, achieve the status of a "Worldwide Health Problem," as the headline of one of Lawrence Altman's articles in the New York Times labeled it in November. By that time, AIDS cases would be reported "in 33 countries and all inhabited continents." Though most cases were in the United States or Europe, the most striking aspect of the epidemic's spread was the discovery of AIDS in equitorial Africa. In April the Washington Post summarized reports appearing in both Lancet and the New England Journal that described cases of AIDS in European countries, but among patients who had immigrated from or traveled in countries such as Zaire and Chad. Of twenty-nine such cases in France, six patients had become ill before June 1981—that is, before the epidemic was first reported in the United States. Immediately
scientists and reporters in the West picked up on the notion that Africa "could have been the breeding place" for the epidemic.
Despite the globalization of the epidemic and the formal change in terminology, the "gay disease" formulation, in various guises, continued to undergird medical investigation of the syndrome through the first half of 1982. For example, an editorial in the Annals of Internal Medicine by Dr. Anthony Fauci, a distinguished scientist who would later become the head of the AIDS program at the National Institutes of Health (NIH), laid out a number of etiological possibilities: "Is there a new virus or other infectious agent that has expressed itself first among the male homosexual community because of the unusual exposure potential within this group? Is this an immunosuppressed state due to chronic exposure to a recognized virus or viruses? Is this illness due to a synergy among various factors such as infectious agents, recreational drugs, therapeutic agents administered for diseases that are peculiar to this population such as the 'gay bowel syndrome' …?" But what Fauci never doubted was that the "critical questions" were: "why homosexual men and why occurrence or recognition only as recently as 1979?"
Suddenly, this whole framework for understanding the epidemic was dramatically challenged. On July 9, the CDC reported thirty-four cases of Kaposi's sarcoma or opportunistic infections among Haitians living in five different states in the United States. None of those interviewed reported homosexual activity, and only one gave a history of injection drug use. The following week the agency reported three cases of PCP in people with hemophilia, all of them recipients of a blood product called Factor VIII, "manufactured from plasma pools collected from as many as a thousand or more donors." The CDC refrained from drawing conclusions, but noted that the occurrence of the hemophilia cases "suggests the possible transmission of an agent through blood products." Since bacteria were screened out of Factor VIII in the production process, while smaller particles such as viruses could potentially escape the screen, the "agent" in question would almost certainly have to be a virus.
Mass, writing in the Native, quickly noted the significance of these findings: of all the existing etiological hypotheses, "only that of viruses would seem able to provide a unitary hypothesis that could explain the sudden appearance of AID [the Native's term at that time] in a growing number of distinct populations." But he also acknowledged the alternative possibility: Perhaps, he suggested, "we are dealing with
a number of superficially similar epidemics, each with its own primary etiology."
Germs and Magic Bullets
One syndrome, one caise; many syndromes, many causes: these options suggested not just different etiological hypotheses, but opposing theoretical approaches to the understanding of human illness. Indeed, one of the most intriguing aspects of the early popularity of the immune overload hypothesis was that so many clinicians would readily forsake the approach to disease causation frequently described as the cornerstone of contemporary biomedicine: the principle of "one disease, one cause, one cure." As Allan Brandt has expressed it: "In this paradigm, individuals become infected with a parasite that causes dysfunction of some sort; disease is defined as a deviation from a biological norm. Social conditions, environmental phenomena, and other variables are generally discounted as causes of disease. The physician dispenses 'magic bullets' that restore the patient to health."
Ever since the bacteriological revolution of the late nineteenth century, when germs replaced "miasmas" as the preferred explanation for illness, medical research typically has focused on the discovery of discrete microbial causes for specific diseases. To be more precise, two separate assumptions have been welded together: that most illnesses have a single, fundamental cause, rather than multiple necessary causes; and that the search for the cause of illness should focus primarily on microbes, very secondarily on lifestyle issues, and only incidentally on environmental causes related to the larger organization of the society. Of course, the monocausal/microbial approach has always had its critics. Writing in 1959, René Dubos characterized the "doctrine of specific etiology" as "unquestionably the most constructive force in medical research for almost a century," but noted that "few are the cases in which it has provided a complete account of the causation of disease." Citing the failures, "despite frantic efforts," to find cures for diseases such as cancer and mental illnesses, Dubos argued that the "search for the cause may be a hopeless pursuit because most disease states are the indirect outcome of a constellation of circumstances. …"
Modern-day epidemiologists, more open to multicausal approaches to disease, may speak of a "web of causation" or may endorse "ecological" and "synergistic" models of illness that emphasize the
complex interrelationships among environmental and host factors. But in laboratories, examining rooms, and medical school classrooms, the doctrine of specific etiology holds sway. Many analysts have seen in the monocausal/microbial model of disease the clue to medicine's ideological function within a capitalist society: it encourages people to attribute their illnesses to invisible particles rather than to occupational hazards or defects of social organization. But to understand why clinicians and researchers themselves reach for such explanations, the suggestions of sociologist Andrew Abbott may be more to the point.
First, the germ theory of disease focuses public attention on medicine's greatest triumphs and away from arthritis, heart disease, cancer, and other chronic problems that have proven less amenable to therapeutic success. Second, one of the chief legitimating values of medicine (like other professions) is its perceived efficiency; and as opposed to environmental explanations, monocausal/microbial ones lend themselves to neat and straightforward solutions ("Take two pills every four hours"). The search for microbes enhances the power of laboratory researchers, who alone have the tools to conduct it. The search for environmental causes is, by contrast, frequently beyond their ken. In short, the commonly expressed preference of clinicians and biomedical researchers for simple, monocausal, microbial models may in an immediate sense have less to do with medicine's role in legitimating society than with doctors' and scientists' roles in legitimating scientific medicine.
In light of the prevailing explanatory preference, early clinical fascination with "the homosexual lifestyle" is all the more noteworthy. Of course, perceptions that illness is linked to lifestyle have become more common in recent years, with increasing attention to the relation between such factors as stress or eating habits and the development of various diseases. But to the extent that doctors endorsed a multicausal lifestyle model, they were going against the prevailing medical currents. It is well worth asking whether they would have been as likely to do so had it not been for the perception that "the gay lifestyle" was peculiarly laden with a potential for medical hazard.
Dissent at the Front Lines
Once put squarely on the table, the notion of a single, unifying cause of AIDS carried with it immediate practical implications.
The virus theory, now described by the Los Angeles Times as "a potentially much more serious candidate for the cause," was also a scary one, as it "raised the specter" of a communicable disease that might potentially affect anyone. Or as Newsweek warned in August, "the 'homosexual plague" has started spilling over into the general population." With the news, toward the end of 1982, of a case of AIDS having developed in a blood transfusion recipient twenty months old (one of whose donors was found to have AIDS) and of other cases in the female sexual partners of intravenous drug users with AIDS, the viral hypothesis gained increasing credibility. It wasn't that the lifestyle theories were immediately abandoned: for example, a news report in the influential Journal of the American Medical Association (JAMA ) surveying the controversy in late September 1982 claimed straightforwardly that "it seems unlikely that a virus alone is inducing AIDS," and devoted significant attention to the poppers theory and others, as well as to two researchers' discovery of a genetic marker in patients with Kaposi's sarcoma. However, the greater the number of risk groups, the less relevant seemed the details of "lifestyle," and the more attractive the notion of a unifying cause that could account plausibly for all manifestations of the syndrome.
In response to this challenge, advocates of the immune overload hypothesis struggled to fortify their claims. A central player was Dr. Joseph Sonnabend, a South African-born physician and researcher. A specialist in infectious diseases, Sonnabend had also done research in England on the drug interferon, put in a stint at Mt. Sinai School of Medicine as an assistant professor of microbiology, and served as the director of venereal disease control for the New York City Department of Health. At the time the epidemic emerged, Sonnabend was practicing as a community doctor in New York's Greenwich Village, largely treating the sexually transmitted diseases of his many gay male patients. Sonnabend had little inclination toward simple, monocausal models of illness. As he would later put it, his South African medical education had stressed that "if you want to understand sickness, you have to understand the environment in which sickness occurs."
Writing in the Native in September 1982, Sonnabend sought support for his views by warning his readers that endorsement of the viral hypothesis could result in antigay discrimination and prejudice: "To publicly propose that any minority group carries a specific infectious agent capable of causing severe immunodeficiency and cancer is an act of tremendous seriousness. Given the potential repercussions, it verges
on the irresponsible that the suggestion is made on the basis of evidence that remains conjectural." The "conjecture," in Sonnabend's view, rested on twin assumptions, both of them debatable: that the same disease was present in "at least four disparate groups" (Haitians, intravenous drug users, hemophiliacs, and gay men) and that the disease was actually new in each group. While Sonnabend was careful to make clear that he was not ruling out these possibilities, his central thrust was to question them by suggesting that there might be various syndromes of immunodeficiency, all with similar symptoms. But rather than attempt to explain the cases of AIDS in the "newer" risk groups, Sonnabend focused attention on immunodeficiency in gay men. He proposed a variant of the original immune overload hypothesis, involving repeated infection with CMV and the reactivation of infection with Epstein-Barr virus. The bottom line, for Sonnabend, was summarized by the title of the Native article "Promiscuity Is Bad for Your Health." "This is not a moralistic judgment," Sonnabend insisted, "but a clear statement of the devastating effects of repeated infections."
As a neighborhood doctor, Sonnabend had limited resources with which to establish credibility, so his first step was to recruit allies. His advantage, as he later saw it, was his location on the front lines: "I was in the situation, as a physician to many of the men who actually developed the disease, to observe the guys in their setting. …" But his problem was that, within the research establishment, he was isolated: "I had this very unique access to information. But it was just myself, a lonely business. There were no takers, because I didn't have an important position in some medical center.… However, I did contact David Purtilo, the chairman of pathology at the University of Nebraska. Purtilo was known to me as an expert on Epstein-Barr virus."
With Purtilo and another researcher, Steven Witkin, Sonnabend published an article in JAMA in May 1983, presenting his claims to a wide medical audience. (This article was later reprinted in the New York Academy of Science's 1984 volume on AIDS, as well as in JAMA 's "official" 1986 anthology of the epidemic, AIDS: From the Beginning .) Challenging the "prevailing view" that a novel infectious agent caused AIDS, the authors reminded their readers of "another acquired immunodeficiency syndrome," called Neapolitan disease, which "resulted from malnutrition and various viral infections." Similarly, the authors contended, multiple factors that included "recurrent
cytomegalovirus (CMV) infections and immune responses to sperm are likely major causative factors" among promiscuous homosexual men. But on the crucial question of other "risk groups," the authors had little to say: "We cannot, at this time, explain why AIDS is thought to be occurring in Haitians, hemophiliacs, and others. Acquired immunodeficiency has many causes, including malnutrition, hormonal alterations, use of opiates and other intravenous drugs, and acute viral infections."
Also in early 1983, Sonnabend became the editor of a new medical journal, AIDS Research , and declared its first issue "an appropriate occasion to review an alternative hypothesis regarding the genesis of AIDS." Here Sonnabend devoted more attention to the other "risk groups," noting that "transfusions are themselves immunosuppressive," since they expose the recipient to a variety of antigens in the donated blood, and that many Haitians are subject to tropical infections, as well as to poverty and malnutrition, both of which are highly correlated with illness. Sonnabend argued that "the risk groups are too broadly defined," and that focused epidemiological research was needed to tease out the specific risk factors (such as exposure to sexually transmitted pathogens in the case of gay men) actually linked to AIDS. Epidemiologists could also assess his model, he suggested, by comparing the prevalence of CMV in populations with and without AIDS.
But Sonnabend had no epidemiologists at the ready, and in the absence of data, his hypothesis was, at best, informed speculation. Much the same could be said about all the "immune overload" theorists. Two years into the epidemic, there was little specific evidence in support of the claim that immune overload caused AIDS in gay men, let alone in other risk groups. Some research had reported on the health effects of poppers, including one study showing that of eight outwardly healthy gay men with signs of T-cell abnormalities, most were consumers of amyl nitrite. But the numbers were too small to warrant strong conclusions. More generally, epidemiologists and statisticians found it "exceedingly difficult to disentangle nitrite use from such other risk factors as the frequency of sexual encounters and the multiplicity of sexual partners." While the interwoven nature of these epidemiologically correlated behaviors could be taken as evidence of an overload model, it could just as easily reflect spurious associations. As Mass pointed out in a discussion of the limits of epidemiological thinking, "On the superficial basis of numbers alone …
wearing handkerchiefed Levi's and having Judy Garland records in one's collection might also seem risky."
Medical Uncertainty and Gay Skepticism
As the number of AIDS cases continued to rise, increasingly fearful gay men struggled to make sense of the shifting and indeterminate medical claims and to sort out the implications for their everyday lives. Toward the end of 1982, Gay Community News (GCN ), a left-leaning weekly based in Boston, cited the "growing consensus among experts that AIDS is transmissible … and most likely through sexual contact." Expressing the paper's sex-positive philosophy, writers in GCN were suspicious of views that blamed gay men for becoming sick, whether voiced by medical authorities or by gay men themselves. One prominent political analyst, Michael Bronski, wrote disapprovingly of the president of Gay Men's Health Crisis, quoting him as saying: "Something we have done to our bodies—and we still don't know what it is—has brought us closer to death." Another writer in the same issue of GCN applauded the views of Jim Geary, head of the Shanti Project, a San Francisco organization: "The reason [we] get sexually transmitted diseases is not because we have multiple sexual partners. … It's because we don't take the necessary precautions in having sex."
The question of how to translate etiological uncertainty into guidelines for personal safety was deeply troubling to gay communities across the United States. Nowhere did the debate rage more fiercely than in the pages of the Native in late 1982. The Native 's editor and publisher, Chuck Ortleb, introduced side-by-side commentaries by stressing the paper's democratic impulse and the need for the general public to assess scientific and public health debates: "The articles printed on these pages provide good examples of the level of debate prevailing in medical circles. … Confusing? Contradictory? Of course. But then, so is much of the discussion surrounding the present health crisis. It's a discussion that we feel virtually everyone should be involved in—gay people as well as non-gay, laymen as well as physicians, policy-makers as well as the citizenry. …"
One view in the debate was offered by Peter Seitzman, president of New York Physicians for Human Rights, the gay doctors' association. His argument was straightforward, if not altogether reassuring:
"The available evidence overwhelmingly suggests that AIDS is caused by some as yet undiscovered transmissable [sic ] agent," probably a virus. Since the transmission pattern appeared to be similar to that of the hepatitis B virus, prevention guidelines would be "precisely the same as those for avoiding hepatitis B," namely, never use a syringe used by someone else and reduce promiscuity. Eager to avoid any implication of antisex attitudes, Seitzman reassured his readers that he himself had been "no more of an angel than Mae West." But he concluded by affirming the virtues of "monogamy as a survival technique," declaring that promiscuity is not immoral "but simply dangerous."
The "opposing" commentary by Michael Callen and Richard Berkowitz in fact arrived at roughly similar, if far more forceful, conclusions, but began with radically different etiological premises. It was also quite different in tone. Callen and Berkowitz identified themselves as twenty-seven-year-old men, both "victims of AIDS," each with a history of having been "excessively promiscuous." Although the article didn't say it, they were also both patients of Dr. Sonnabend and they endorsed his immune overload hypothesis. (Callen would go on to become the most prominent "long-term survivor" of AIDS in the United States, a familiar figure at rallies and demonstrations; until his death in 1993, he remained an activist and an ally of Sonnabend's.) Entitled "We know Who We Are: Two Gay Men Declare War on Promiscuity," the article was nothing short of a manifesto: "Those of us who have lived a life of excessive promiscuity on the urban gay circuit of bathhouses, backrooms, balconies, sex clubs, meat racks, and tearooms know who we are. … Those of us who have been promiscuous have sat on the sidelines throughout this epidemic and by our silence have tacitly encouraged wild speculation about a new, mutant, Andromeda-strain virus. We have remained silent because we have been unwilling to accept responsibility for the role that our own excessiveness has played in our present health crisis. But, deep down, we know who we are and we know why we're sick."
Turning to the medical evidence in favor of the different causal hypotheses—which they had evaluated on the basis of "personal experiences," their talks with researchers and doctors, and their "own readings in both the medical and the lay press"—Callen and Berkowitz argued that "AIDS is not 'spreading' the way one would expect a single-viral epidemic to spread." The confinement of AIDS to specific risk groups, they maintained, should lead us to look for the specific
explanation for each group's immunosuppression. In practical terms, whatever theory one chose to believe, "the obvious and immediate solution to the present crisis is the end of urban male promiscuity as we know it today," the authors concluded. "The party that was the '70s is over," and anyone who defended promiscuity on political or ideological grounds was simply in denial.
Sharp responses to Callen and Berkowitz were quickly forthcoming, both in the Native and in other lesbian and gay publications. Charles Jurrist, writing "In Defense of Promiscuity," argued in his reply that the uncertainty of scientific knowledge about causation had to be factored into any evaluation of personal risk. While granting that the immune overload hypothesis "is the most plausible of the several theories concerning the origins of AIDS," Jurrist reminded readers that the hypothesis was far from proven: "It therefore seems a little premature to be calling for an end to sexual freedom in the name of physical health."
Others, such as Michael Lynch, writing in the pages of the Canadian lesbian and gay newspaper The Body Politic , were even more assertive in defending sexual freedom against medical moralism. These writers put the issue in historical and political context: The medical critique of gay promiscuity was simply the latest of many attempts to portray gay sexuality as diseased. At stake in the debate was "gay identity" itself. Gay men had fought to construct an affirmative identity, an essential part of which involved strong defense of sexual freedom and a critique of puritanical attitudes. And many of those they had fought against were doctors and medical researchers. Given this history, it followed that the debate about gay men and their sexual practices was thoroughly interwined with an older power struggle: who was to say what it meant to be gay—the doctors, or gay men themselves? As Lynch poignantly expressed it: "Like helpless mice we have peremptorily, almost inexplicably, relinquished the one power we so long fought for in constructing our modern gay community: the power to determine our own gay identity. And to whom have we relinquished it? The very authority we wrested it from in a struggle that occupied us for more than a hundred years: the medical profession."
In the absence of a cure for AIDS, or even an agreed upon cause—and in the aftermath of an initial scientific framing of AIDS as a "gay disease" linked to promiscuity, a formulation that aroused the wrath of many in gay and lesbian communities—the credibility of doctors,
biomedical researchers, and public health authorities suffered greatly in those communities. Increasingly gays were prompted to respond by insisting on their own right to intervene—to weigh the evidence, pass judgment, and remind the medical establishment at every pass whose lives were really on the line. Gay doctors like Mass sought a moderate position; writing in the Native in response to Lynch's commentary in The Body Politic , he acknowledged: "To an enormous extent, what Lynch is saying is true. Mainstream medicine and psychiatry have in fact been largely responsible for contemporary stereotypes of homosexuals as 'abnormal,' 'perverse,' and 'sick.' At the same time, however, mainstream medicine and psychiatry continue to serve vital health needs." Maintaining that the problem was not with medical science but with "the political abuse of that science," Mass advised his readers to "be critical but remain open to well-qualified medical advice." But for those on either extreme of the promiscuity debate, from Lynch to Callen and Berkowitz, the watchword was self-reliance. Become your own expert: ultimately, that was the only reasonable hope gay people might have of surviving. "Rely on no single source for your information," exhorted Callen and Berkowitz: "not your doctor, not this newspaper, not the Gay Men's Health Crisis, not the Centers for Disease Control."
Of course, it goes without saying that this strategy of collective empowerment presumed the existence of gay doctors, gay newspapers, and a Gay Men's Health Crisis. To be sure, the spreading disease would decimate the ranks of existing gay leadership. But ironically, the gay response to AIDS both presupposed and furthered the social development of lesbian and gay communities and their political clout—a process that Dennis Altman has called "legitimation through disaster." Gay men and lesbians had long confronted homophobic attitudes, antigay discrimination, and heterosexist presumption on a daily basis in the workplace, in religious settings, in encounters with family members, on television, and in the movies. But in organizing to meet these challenges, lesbians and gay men had developed political and social institutions that were poised to respond to the new threat when it erupted. Moreover, gay communities were dominated by white, middle-class men—people with influence in society and access to an array of social, cultural, and political resources. It's no surprise that gays were hotly debating the details of causation theories while intravenous drug users—often the poorest of the poor—sat on the sidelines: these were the realities of power in the United States in
the 1980s. Even people with hemophilia, a diverse group that had the benefit of a preexisting national lobby, did not mobilize forcefully in response to the emergence of the epidemic. In this early period, Haitians were the only other group to challenge medical claims; they objected to the portrayal of Haiti as a possible origin of the epidemic and combated wild epidemiological speculation about the role of voodoo rituals in the transmission of AIDS. And most of the opposition came not from the grassroots but from politicians in Haiti and Haitian doctors living in the United States.
The distinctiveness of gay communities' approaches to the emergence of the epidemic is brought out in Cathy Cohen's comparative analysis of gay and African-American responses. Although gay communities were hit harder, both gays and African-Americans came to be disproportionately represented in the statistics of illness and death as the epidemic proceeded. Both of these social groups were marginalized, and historical memory inclined both of them to distrust federal biomedical institutions. Yet "the indigenous norms and structures of these communities" promoted different political outcomes: "In the Gay community AIDS has become associated with the community's struggle for rights and entitlements. In the Black community much of the response to AIDS is based on a framing of the disease that still emphasizes behavior and the individual actions of those who have AIDS, making it much more difficult to transform AIDS into a political issue for the community." As Cohen has described, established African-American organizations eschewed "ownership" of the problem of AIDS. It was often up to black gays and lesbians—those who stood at the intersection of these two social groups—to try to mobilize African-American communities and start up new organizations, while simultaneously confronting racism within gay communities.
The Triumph of Retrovirology (1982–1984)
Gallo's Family of Viruses
Writing in 1988, Robert Gallo, the NIH scientist who would share credit for discovery of what was to become known as the "human immunodeficiency virus," reflected back on the scientific effort to understand AIDS. Gallo concluded that progress had been made possible by "two general earlier developments": "first , by major advances that took place in basic sciences, particularly in immunology
… and molecular biology …; and second , by the opening of the whole field of human retrovirology that, oddly enough, occurred only a few years before the AIDS epidemic. …" To this Gallo added, "There is no doubt in my mind that if AIDS came upon us full force in the 1960s or even in the early 1970s, we would still be wandering in the dark regarding most of what we know today."
Gallo's "odd" fact can be put in different terms: At the moment when people began to suspect that AIDS might be caused by an infectious agent, there existed a small group of prominent scientist working in a very specialized area who were inclined to imagine that a "retrovirus" might be the cause, who were motivated to pursue that speculation, and who were well equipped to do so. Only in the 1960s had researchers discovered that the genetic material of certain viruses consists of RNA (ribonucleic acid) rather than DNA (deoxyribonucleic acid, often called the "blueprint of life"). Normally, viruses infect cells and turn them into virus factories, causing the cells to produce new viruses according to the specifications of the rival DNA. The virus's DNA is copied into RNA, which is then used to manufacture viral proteins; once the new viruses are assembled, they are ejected and go off to infect other cells. When viruses were found that consisted of RNA rather than DNA, they presented a puzzle to scientists, because it was unclear how the viruses could replicate. In 1970, however, in work that would win them the Nobel Prize, researchers David Baltimore at the Massachusetts Institute of Technology and Howard Temin at the University of Wisconsin independently discovered that these RNA viruses contained an enzyme, which they termed "reverse transcriptase," that copied the viral RNA into DNA. This DNA then served as the blueprint for the manufacture of new viruses. So while in normal viruses the sequence was "DNA to RNA to new viruses," in these unusual viruses there was an extra step: "RNA to DNA to RNA to new viruses." To describe the transcription from RNA to DNA and back again, virologists coined the term "retrovirus."
During the "War on Cancer" in the 1970s, researchers such as Gallo at the NIH's National Cancer Institute (NCI) investigated links between animal retroviruses and various forms of cancer. However, until the late 1970s, no retroviruses were known to cause disease in humans. At that time, both Gallo and a group of Japanese researchers claimed credit for the discovery of one believed to cause adult T-cell leukemia, a rare form of cancer found mostly in Japanese fishing villages. Gallo named the retrovirus the human T-cell leukemia virus,
or HTLV. This work earned him the Lasker Prize, the highest award in biomedicine short of the Nobel Prize. He found another virus in the same family in 1982, which he claimed caused a different type of leukemia; in consequence, the two viruses became known as HTLV-I and HTLV-II.
As Gallo described it in retrospect, when he first heard about the new syndrome in gay men in 1981, he had no reason to think it might be linked to a retrovirus and indeed had little interest in the issue. Or as Joan Fujimura has suggested more generally, scientists construct and pursue "do-able problems": they do not venture off in any direction at random, but rather structure their work by finding effective ways of integrating and coordinating the relationship between the experimental procedures at hand, the organization of their laboratories, and the social worlds through which they move. Given that the initial hypotheses focused on homosexual lifestyle risks, many virologists simply saw no particular reason to be interested.
By Gallo's account, his curiosity was piqued only in 1982, when James Curran of the CDC briefed NIH researchers about the epidemic, expressing to them his own belief that the syndrome was caused by an infectious agent, and stressing that one hallmark of the syndrome was the helper T-cell deficiency. This was enough for Gallo to hypothesize that the epidemic might be caused by HTLV or by a retrovirus of the HTLV family—by a close relative, that is, of the two viruses whose discovery had already brought him considerable acclaim within the world of virology. After all, HTLV specifically infected helper T cells; moreover, HTLV was known to be transmitted in blood and semen, which seemed also to be plausible transmission routes of the putative agent in AIDS. Finally, there was some precedent for a retroviral role in a condition like AIDS, since a feline retrovirus was linked to immune deficiency in cats. Gallo became convinced that AIDS was an HTLV-linked disease. Only some years later would he do an about-face and make an intriguing confession: "That hypothesis, as it turned out, was wrong. Nonetheless, it was fruitful, because it stimulated the search that led to the correct solution."
Gallo had little patience for alternative hypotheses that were common at the time. The medical tendency to, as he put it, "round up the usual suspects"—CMV, Epstein-Barr virus, and the like—seemed to him unlikely to provide an explanation for what was, after all, a new epidemic. Nor was he impressed by the popular hypothesis of immune overload. Interestingly, he objected not just on empirical grounds—that
immune overload seemed unlikely to account for manifestations in all the risk groups—but also on the basis of his understanding of causality in disease processes: "Whereas some complex diseases … are believed to involve different steps and sometimes different factors, most human disease (even some cancers) can be thought of as involving a primary causal factor. Certainly this has been the case for most past epidemic disease for which we in time did learn the cuase."
Committed in general to what Dubos called the "doctrine of specific etiology," Gallo dedicated his laboratory to an investigation of his hypothesis: that AIDS was caused by the virus he was already working with and had invested in, HTLV. Within weeks of embarking on this search, Gallo's assistants found the leukemia virus in the T cells of two U.S. gay men, a Haitian woman who died of AIDS in France, and a Frenchman who had received a blood transfusion. Gallo sent two papers describing the findings to Science magazine, the preeminent general science publication in the United States. His colleague, Myron ("Max") Essex at the Harvard School of Public Health, sent along a third paper also reporting signs of HTLV infection in AIDS patients.
The French Virus
Meanwhile, across the Atlantic, a similar search for a retroviral cause of AIDS was proceeding according to different premises. In Paris, a group of physicians had been meeting informally to discuss the epidemic, and one of them, an immunologist named Jacques Leibowitch, who was familiar with Gallo's work on HTLV, had become convinced that a retrovirus was the cause. Skeptical of arguments about poppers and promiscuity, Leibowitch specifically hoped to demonstrate "that the cause of AIDS was not homosexually related." But neither Leibowitch nor any of his colleagues knew how to look for a retrovirus, so they set out to enlist the support of Luc Montagnier, chief of viral oncology at the famous Pasteur Institute, a private, nonprofit research institution founded by Louis Pasteur in 1887.
The physicians' group had a hunch that if a virus was causing the depletion of T cells, then there might be higher levels of virus present in people who were at an earlier stage of illness, before most of their T cells had been killed off. So they sent Montagnier samples of lymph tissue from a gay male patient with "lymphadenopathy syndrome"—a
condition of chronically swollen lymph glands, increasingly prevalent among gay men and believed by many to be a precursor to AIDS. Montagnier's research team extracted T cells from the tissue and put them in an incubator with nutrients, hoping to grow a virus. When tests showed the presence of reverse transcriptase, the enzyme that is the distinctive marker of retroviruses, they knew they had found something. The reverse transcriptase activity rose and then fell—a sign that the virus was killing its host cells—but by adding fresh cells from new sources, the French researchers were able to maintain the culture. With the aid of electron microscopy, the Pasteur group also succeeded in photographing viral particles.
When Montagnier contacted Gallo in early 1982 and informed him of his findings, Gallo encouraged him to submit his paper to Science , so that Gallo's, Essex's, and Montagnier's papers could all appear together. Since Science allows its authors to suggest appropriate peer reviewers, Gallo told Montagnier he would be happy to review the Pasteur Institute;s findings for the magazine. In his comments to Science , Gallo urged rapid publication, stressing the importance of Montagnier's work. But in addition, as reported John Crewdson has described in a highly critical exposé of Gallo's work, Gallo offered to write the abstract, which Montagnier had neglected to include. Gallo's abstract identified the French virus as a "C-type retrovirus," similar to Gallo's HTLV. Gallo had effectively enlisted the Pasteur researchers behind his own HTLV.
The papers appeared in Science in May 1983, where, as Crewdson noted, they "made a considerable splash." But few people paid much attention to Montagnier's paper, which followed the other three in the pages of Science ; it appeared simply to confirm the findings of the American researchers. As Jay Levy, a virologist at the University of California at San Francisco Medical School (UCSF), who had also embarked on a search for a retroviral causative agent, later recalled, "The write-up in the Science papers sounded like the French virus and the Gallo virus were the same."
But Montagnier and his collaborators suspected otherwise. Their photographs didn't especially resemble HTLV. And when they exposed their virus to HTLV antibodies, they didn't observe any "cross-reaction"—as they should have, if the virus were really a close cousin of HTLV. Most crucially, their virus killed T cells in the test tube. HTLV caused its host cells to multiply wildly—the hallmark of cancer. Of course, the French had no actual proof at this point that the virus
they had found was indeed the cause of AIDS. But they were increasingly convinced that theirs was a previously undiscovered retrovirus, not HTLV or even a member of the same family; and they set out to demonstrate its causal relationship to the epidemic.
By fall 1983, at the virology conference held each September in Cold Springs Harbor, New York, Montagnier could report finding his virus—which he was now calling "LAV," or lymphadenopathy-associated virus—in about 60 percent of patients with lymphadenopathy syndrome and 20 percent of those with AIDS. None of these patients appeared to be infected with HTLV. At the conference, Gallo angrily disputed Montagnier's findings, claiming that the French measurements had to be in error. (Much later, Gallo would write: "I have come increasingly to regret that the tone or spirit of my questioning that day was too aggressive and therefore misunderstood.") What Gallo did not mention to the conference-goers was that, despite his own lab's best efforts, he and his associates had been unsuccessful in finding HTLV in the majority of samples from AIDS patients that they had been studying over the past several months.
An Addition to the Honor Roll?
The events of the subsequent seven months are obscure, and—despite intensive scrutiny by journalists and a half dozen official investigations by various reputable bodies—the facts may never fully be known. What appears beyond dispute is that, shortly after the Cold Springs Harbor conference, Montagnier forwarded to Gallo a sample of LAV for him to study. Then, the following April, reports of Gallo's discovery of a "third variant" of HTLV began to appear in the pages of U.S. newspapers. Just months after insisting that HTLV was the cause of AIDS—while increasingly having trouble finding it in AIDS patients—Gallo presented the world with a new virus, "HTLV-III," which he claimed was a member of the HTLV family. Later, in January 1985, investigators would determine that Gallo's HTLV-III samples had a 99 percent genetic similarity to Montagnier's LAV—that is, the viruses were much too similar to have come from separate sources. The implications were clear: Whether the consequence of accidental contamination of viral cultures—a common problem in virology labs—or of outright theft and misrepresentation, the Pasteur Institute's LAV had found its way into Gallo's cultures. Almost beyond a doubt, Gallo had in fact "discovered" Montagnier's virus.
Yet none of this was known in 1984. Indeed, there was little said about Montagnier on April 23 that year, when Margaret Heckler, President Ronald Reagan's secretary of health and human services, stood before a roomful of reporters. "The probable cause of AIDS has been found," she announced with some fanfare: "a variant of a known human cancer virus, called HTLV-III." Just a few days earlier, Lawrence Altman, the New York Times 's medical reporter, had received a scoop from CDC Director James Mason, who told him that a virus discovered in France, called LAV, was the likely culprit; the Times had run the story on the front page. "There was so little excitement in the scientific community when the French came up with their announcement last May," noted Mason, claiming he did not understand why it had taken so long for the importance of the Pasteur Institute's work to be recognized. But at the press conference on Tuesday, Mason's boss had a different tune to play.
"Today we add another miracle to the long honor roll of American medicine and science," said Heckler. "Those who have said we weren't doing enough," she added, in response to widespread complaints of inactivity on AIDS by the Reagan administration, "have not understood how sound, solid, significant medical research proceeds." As Randy Shilts described it, the researchers on the podium with Heckler "blanched visibly when she proclaimed that … a vaccine would be ready for testing within two years."
Heckler made only brief reference to the Pasteur Institute scientists, describing them as "working in collaboration with the National Cancer Institute"; she indicated her belief that LAV and HTLV-III "will prove to be the same." Nor was mention made of UCSF virologist Jay Levy, who was also close on the heels of a virus linked to AIDS. (He would submit his paper to Science the following month.) Pressed by puzzled reporters, Gallo added: "If it [the virus] turns out to be the same I certainly will say so…." Heckler emphasized the crucial role of the U.S. research, noting that only Gallo had succeeded in reproducing large quantities of the virus, which was necessary for the development of a blood test that could detect viral antibodies. Hours earlier, the U.S. government had filed a patent application for just such a test.
The New York Times , in an editorial printed a few days afterward, was not slow to draw implications from the episode. "In the world of science, as among primitive societies, to be the namer of an object is to own it," the Times noted wryly, pointing to the dispute between
"LAV" and "HTLV-III." Since the blood screening test was not yet in commercial operation and no vaccine had yet been produced, "what you are hearing is not yet a public benefit but a private competition—for fame, prizes, new research funds."
"Strong Evidence of a Causative Involvement"
Certainly one of many unusual aspects of the whole affair was that Heckler's press conference was held before Gallo's findings had even been published in a peer-reviewed forum—normally a serious breach of professional scientific etiquette in itself. Those who wanted more substantial information about Gallo's claims had to wait until May 4, when four articles by Gallo's group appeared in the pages of Science . This too was extraordinary. As Gallo later commented, "Getting one paper in Science is a lot. Getting two is fantastic. Getting three was a record. We had four at one time."
Gallo used these articles to put forward a series of interconnected claims: that he had found a new virus; that he had succeeded in mass-producing it; that the virus was related to HTLV; that antibodies to the virus could be detected in blood; and, most crucially, "that HTLV-III may be the primary cause of AIDS." In the second of the four papers, Gallo and his coauthors focused specifically on the etiological argument. After reviewing the evidence in favor of an infectious agent as the cause of the syndrome, Gallo reminded his readers that "we and others have suggested that specific human T-lymphotropic retroviruses (HTLV) cause AIDS." Gallo's wording was also significant: he had redefined HTLV, from "human T-cell leukemia virus" in 1983, to "human T-lymphotropic retroviruses " in 1984. While the original name denoted the relation between a single retrovirus and a specific form of cancer, the new name described a family of viruses more vaguely characterized as "T-lymphotropic," that is, having an affinity for T cells. Gallo had reinvented "HTLV" so as to more plausibly encompass his new virus as a relative of HTLV-I and HTLV-II.
Moving on to HTLV-III, Gallo described detecting the virus in, and isolating it from, "18 of 21 samples from patients with pre-AIDS [the so-called lymphadenopathy syndrome], three of four clinically normal mothers of juvenile AIDS patients, three of eight juvenile AIDS patients, 13 of 43 … adult AIDS patients with Kaposi's sarcoma, and 10 of 21 adult AIDS patients with opportunistic infections." Although
ideally one would expect to find a primary causative agent in every case of a disease, Gallo noted that "the incidence of virus isolation reported here probably underestimates its true incidence since many tissue specimens were not received or handled under what we now recognize as optimal conditions." In contrast with these findings that associated the virus with the expression of AIDS was the striking absence of HTLV-III in cases where AIDS was also absent. Out of 115 clinically normal heterosexual blood donors, not a single one showed signs of the virus. And out of 22 clinically normal gay male donors, only one tested positive for the virus, and that person developed AIDS within six months. These studies, Gallo and his coauthors concluded, "provide strong evidence of a causative involvement of the virus in AIDS."
What in fact had Gallo established? Four years later, in response to challenges about whether the virus had been proven to cause AIDS, Gallo would maintain: "In my opinion all of the sufficient data was available at the time the cause was first announced in the spring of 1984." But this was a difficult position to sustain, at least on the basis of Gallo's published findings. Gallo had shown that, in specific small samples, laboratory signs indicating the presence of his virus were often correlated with the expression of AIDS at what were believed to be two different stages of disease progression ("pre-AIDS" and AIDS). Moreover, there were no such signs of virus in clinically normal people, suggesting that the virus or viruses had some special relationship to AIDS. But just because HTLV-III and LAV were often correlated with the syndrome, did that mean they were causing it? AIDS, after all, was a syndrome whose hallmark was the presence of a range of opportunistic infections; perhaps HTLV-III and LAV were viruses that were contracted by people who already had weakened immune systems. Gallo would have been in a better position to respond to this challenge if he had had more cases like that of the clinically healthy but infected gay man who later developed AIDS. But the other 21 of his 22 "clinically normal homosexual donors" all tested negative for the virus, so there was really no evidence that HTLV-III infection was a precursor to immune system damage. (Three out of 4 of the "clinically normal mothers of juvenile AIDS patients" tested positive for the virus, but these numbers were small, and Gallo did not report that any of the women had subsequently developed AIDS symptoms.)
When asked ten years afterward whether he had been able, at
the time of publication, to rule out the possibility that HTLV-III was an opportunistic infection, Gallo acknowledged that he could not. But "the evidence was overwhelming in my mind," Gallo recalled. "Science is never 100 percent. It's not mathematics. You play not on hunches, but on data that becomes overwhelming in your mind. …" To make a credible claim for "strong evidence of a causative involvement," Gallo was in fact relying heavily on the plausibility of HTLV-III as a pathogenic agent, given what was known about the virus and about AIDS. At least in vitro, HTLV-III killed helper T cells. And the central manifestation of immune system damage in people with AIDS was precisely the low numbers of those same helper T cells. Still, at this point, little was known about the effects of HTLV-III in vivo.
Koch's Postulates and the Proof of Causation
Epidemiologists and biomedical researchers rely on a range of principles to establish causation in disease. However, since the acceptance of different versions and interpretations of these principles of causation has itself become one of the stakes in the controversy over the causation of AIDS, these principles cannot be independently invoked as neutral measures. The most well known causation criteria are called "Koch's postulates," named after Robert Koch, the nineteenth-century German microbiologist. The postulates consist of four steps that are easily stated. First, the causal agent must be found in all cases of the disease. Second, the agent must be isolated from a carrier and grown in pure culture. Third, when the culture is injected into a susceptible laboratory animal, the animal must contract the disease. Finally, the causal agent must then be recovered from the diseased animal.
The precise relevance of Koch's postulates to contemporary biomedical research (particularly with regard to viruses, which were unknown at the time of Koch's own work) is in dispute, and this dispute has been magnified as a result of recent debates about the causation of AIDS. Many have proposed that researchers nowadays must work with "modern" or revised versions of the postulates, and have argued that Koch himself did not intend them to be followed rigidly. Nevertheless, Koch's postulates remain a well-known reference point for considering questions of etiology in scientific medicine.
For instance, Richard Krause, the director of the National Institute of Allergy and Infectious Diseases of the NIH, gave a conference talk in the summer of 1983 on "Koch's Postulates and the Search for the AIDS Agent," noting that "technical difficulties" often "impede the fulfillment" of all of Koch's postulates, but concluding: "If we abide by the scientific guidance of Koch's postulates, we are sure to discover the cause of AIDS." Similarly, Lawrence Altman focused squarely on Koch's postulates in an article, published later in 1984, on "How AIDS Researchers Strive for Virus Proof." Altman presented Koch's postulates as an important medical tradition that researchers have looked to for a century, but he noted that doctors are sometimes forced to rely on immunological or other experimental evidence when Koch's postulates cannot fully be satisfied. With less equivocation, James D'Eramo wrote in the New York Native soon after the Heckler press conference: "The definitive classical proof that a virus or bacterium causes disease rests on causing the disease in animals by injecting them with the putative agent. AIDS has yet to occur in a laboratory animal." Dr. Nathan Fain, the medical writer for the national, West Coast-based gay newsmagazine the Advocate, made roughly the same claim in May when he explained why "work must continue to prove beyond all doubt that the candidate virus does cause AIDS."
Clearly, if Koch's postulates are the benchmark, then Gallo's May 1984 articles in Science by no means established HTLV-III as the cause of AIDS. But since the criteria for proving causation have been contested, it may be useful to assess the credibility of Gallo's claims-making by looking at a relatively weak version of the causation criteria presented in a recent epidemiology textbook. According to Mausner and Kramer, the likelihood that an association is causal can be evaluated by examining several criteria. First, there is the strength of the association, which they describe as the "ratio of disease rates for those with and without the hypothesized causal factor": here Gallo's evidence is compelling but far from perfect, since he was able to isolate the virus only in fewer than half of the samples from people actually diagnosed with AIDS. Second, the "dose-response relationship": does a higher dose of the causal factor result in higher rates of disease expression? Gallo had no data on this point. Third, the consistency of the association across different studies: clearly this was yet to be determined. Finally, is the association a "temporally correct" one, meaning that the cause precedes the expression with a sufficient "induction period" or "latency period"? With the exception of the
one virus-positive, clinically healthy gay man who developed AIDS within six months, Gallo had no relevant data to report.
Given the state of the evidence in early 1984, perhaps a more plausible claim was that of Jay Levy, whose results in isolating what he called "ARV," or AIDS-associated retrovirus, were published in August. Levy found signs of ARV in about half his AIDS patients and in about 20 percent of clinically healthy homosexual men, but in only 4 percent of clinically healthy heterosexuals. Levy recalled agonizing over how to phrase his conclusion: "I called a good friend of mine … who's an editor, and I said, 'How do I do this? I don't want to say it isn't, but I don't want to say it is .'" In the end, Levy's wording was cautious: "Although no conclusion can yet be made concerning their etiologic role in AIDS, their biologic properties and prevalence in AIDS patients certainly suggest that these retroviruses could cause this disease."
But for Gallo, the notion that he had proven the virus to be the cause became something crucial to defend, particularly as his credibility on other claims was challenged. In 1985, the Pasteur Institute sued the U.S. government in a patent dispute over the discovery of the virus, and in 1987 the heads of the two governments, Jacques Chirac and Ronald Reagan, signed an agreement splitting the royalties for the commercial antibody test. Especially after it became apparent that Montagnier's LAV had found its way into Gallo's viral cultures—a point that Gallo would formally concede in 1991—Gallo gradually backed off from claiming any primacy. And although Gallo continued to present the discovery of HTLV-III as a natural outgrowth of HTLV research, he was eventually forced to accept the prevailing view that, from a genetic standpoint, the new virus was not reasonably classifiable as an HTLV virus. In response to the confusing array of acronyms then in use—HTLV-III, LAV, ARV, HTLV-III/LAV, and others—the Human Retrovirus Subcommittee of the International Committee on the Taxonomy of Viruses rebuffed Gallo and agreed on a new, compromise, name in 1986: HIV, human immunodeficiency virus. (Levy and Montagnier signed the agreement; Gallo and his close associate, Max Essex, dissented.)
The Framing of AIDS
The naming of the virus by the Human Retrovirus Subcommittee marked the initial stabilization of "HIV" as a unitary
object of medical knowledge. But even before this point, the illness AIDS had become a relatively stable cultural entity whose social meanings, however fluid and multiple, had at least begun to congeal. Over the course of a few years, AIDS had come to be "framed," or constructed, within the context of strong beliefs and attitudes about sexuality, promiscuity, and homosexuality and through recourse to a wide range of analogies: Was AIDS like cancer? Was it like herpes? Was it like hepatitis B? Was it an HTLV-like illness? AIDS itself had also come to serve as a frame for understanding other events and social behaviors. Perhaps most notably, as sociologist Steven Seidman has argued, "AIDS … provided a pretext to reinsert homosexuality within a symbolic drama of pollution and purity."
These framings, and the associated stigma, had also provided possibilities for gay men to assert claims for "ownership" of the epidemic (however ambivalently), or at least some of the public responses to it. Indeed, the same social networks and institutional linkages that had permitted rapid amplification of a virus also gave rise to the organization of a concerted grassroots response. Lesbians, subject to what Erving Goffman has called a "courtesy stigma," or stigma by association, acted as collaborators with gay men in these efforts, often playing leadership roles. This extraordinary success of gay and lesbian communities in establishing their right to speak about the epidemic would fuel a willingness and capacity to challenge the knowledge-making practices of biomedicine in the coming years.
Biomedical researchers, and in particular virologists, had also staked out claims to "ownership" of AIDS, and had done so through powerful findings concerning a probable causal agent. The credibility of AIDS research would rapidly become linked to the credibility of this particular causal claim: between 1984 and 1986, the retroviral hypothesis would achieve near-hegemonic status among scientists. It would also, by and large, be taken for granted in the communities affected by the epidemic, in the mass media, and among the lay public. The pathways, mechanisms, and consequences of the "black-boxing" of HIV are the topics of the next chapter.
HIV and the Consolidation of Certainty
The Construction of Scientific Proof (1984–1986)
The Blossoming of AIDS Research
Scientific research on AIDS expanded at a rapid clip during the mid-1980s. From only a couple dozen publications in 1982, the literature grew by more than six hundred new publications in 1983, eleven hundred in 1984, sixteen hundred in 1985, and twenty-seven hundred in 1986. The annual growth rate ranged between 47 and 75 percent, at a time when the level of biomedical publication in general increased at a rate of only 3 or 4 percent a year. In 1982, AIDS articles appeared in three different languages and were published in the journals of five different countries; the 1985 contributions, by contrast, included forty-three countries and twenty-one languages (however, articles were published predominantly in the English language, in U.S. and British journals).
That AIDS research became a scientific growth industry in these years is not surprising in itself. After all, the exponential curve of the cumulative scientific literature roughly matched the exponential curve of the cumulative number of AIDS cases reported to the World Health Organization. That is, the development of scientific interest in AIDS simply paralleled the epidemic's toll. But these general statistics on
overall growth of the literature do not tell the full story. The official announcement of the discovery of the probable cause of AIDS, marked by the Heckler press conference and the publication of Gallo's articles in Science , dramatically transformed the nature of published research on AIDS.
Some specific numbers suggest this transformation. Fully a quater of all 1983 publications on AIDS were concerned, at least in part, with the topic of etiology. By 1985 the number had declined to about 10 percent and by the following year to about 5 percent. The percentages can be deceptive: in absolute numbers there continued to be a constant production of about 150 papers a year that discussed etiology. But in relative terms these papers came to constitute a smaller and smaller fraction of the whole. Meanwhile, during the same period, the percentage of papers concerned with the virus soared, rising from 2 percent in 1983, to 5 percent in 1984, to 20 percent in 1985, to 37 percent (almost 2,000 publications) in 1986. (Research focusing on "the virus" included articles on HIV under its various apparent guises, such as HTLV-III, LAV, and ARV, as well as articles on "HIV-2" ["HTLV-IV," "LAV-2," and so on], a second retrovirus linked to AIDS, discovered by Montagnier in West Africa in October 1986. With the discovery of HIV-2, the original virus was dubbed "HIV-1," although many continued to refer to it simply as HIV.)
Interest in etiology trailed off, while interest in the virus itself exploded: these facts, taken as a whole, are consistent with what is intuitively apparent—that the hypothesis "HIV causes AIDS" enjoyed a rapid and successful transition to the status of scientific fact. But this leaves many questions unanswered. Why did other scientific writers come to accept Gallo's claim? What evidence was considered? What evidence was disputed? What additional evidence, if any, proved decisive in the minds of researchers? Did anyone challenge the reigning hypothesis?
Citation and the Construction of Facts
Paula Treichler, a discourse analyst and cultural critic, has questioned the realist presumption that the HIV hypothesis became fact simply "because it's true." With reference to Gallo and his close associates, Treichler has argued: "By repeatedly citing each other's work, a small group of scientists quickly established a dense citation
network, thus gaining early (if ultimately only partial) control over nomenclature, publication, invitation to conferences, and history."
Yet Treichler provided neither evidence nor elaboration to support this claim. To consider the acceptance of Gallo's hypothesis more carefully, I performed a content analysis of those scientific articles published in seven major journals in 1984, 1985, and 1986 that cited Gallo's crucial 1984 article published in Science (the one specifically advancing the causal argument). Within the pages of these journals during the period 1984–1986, there were 244 articles that cited Gallo, ranging from 19 in Nature to 66 in Science . These were the pivotal years, as evidenced by the citation trend in all scientific publications: Gallo's article was cited 116 times in 1984 and 410 times in 1985; this dropped off slightly to 384 citations in 1986 and then more sharply to 341 citations in 1987 and 284 citations in 1988. Like most influential scientific articles, Gallo's enjoyed a brief period of heavy use during which more and more people found reason to invoke it—after which point the claims enunciated within it presumably became too much a part of common knowledge for citation to be necessary.
In my content analysis I investigated four factors: first, whether scientists and clinicians referenced Gallo's article in order to support qualified claims about the causal role of the virus ("HIV is the virus widely believed to cause AIDS") or unqualified claims ("HTLV-III, the etiological agent in AIDS, …"); second, whether qualified and unqualified claims were made more (or less) frequently over time; third, whether articles authored or coauthored by Gallo or any of his 1984 coauthors were more (or less) likely to make unqualified claims than those written by other authors; and fourth, whether the articles that made unqualified claims were more likely to cite later articles in conjunction with Gallo's in order to back up those claims. (For details on how this analysis was carried out, see the Methodological Appendix.)
Table 1 shows a striking shift over the three-year period. Only 3 percent of the 1984 articles that cited Gallo (2 out of 59) did so in conjunction with unqualified claims about the virus being the cause. Fifty-eight percent of them cited Gallo to support qualified claims, while 34 percent cited Gallo for other reasons and without making etiological claims. By the following year, the percent citing Gallo to make unqualified claims had jumped to 25 percent (26 out of 106). And by 1986, 62 percent (49 out of 79) of the articles cited Gallo to make unqualified claims, and only 22 percent did so in conjunction with qualified claims.
A glance at some of the more authoritative sources within the sample reveals the trend over time. A review article by the Council on Scientific Affairs of the AMA, published in October 1984, spent nearly two pages reviewing various etiological hypotheses and then concluded: "At the present time, the retrovirus etiology of AIDS is the hypothesis for which there is the most convincing evidence." However,
"even though the time may be close at hand when the definitive cause of AIDS is established, there is yet much to be explained." The authors noted several questions: "Why has AIDS been largely confined to certain groups while the majority of the population does not appear to be at much risk of acquiring the disease? Why does frank AIDS develop in only a small percentage of patients with the lymphadenopathy syndrome?" A year later, several prominent epidemiologists from the CDC wrote an article for Science reviewing the literature on the epidemiology of AIDS, noting in the opening paragraph that, in 1984, "a retrovirus variously termed lymphadenopathy-associated virus (LAV), human T-lymphotropic virus type III (HTLV-III), or AIDS-associated retrovirus (ARV) was isolated and shown to be the cause of AIDS [emphasis added]." Similarly, a group of investigators with the Division of Virology of the Food and Drug Administration (FDA) wrote in the Annals of Internal Medicine in late 1985: "The role of the human T-lymphotropic virus type III (HTLV-III) in the development of the acquired immunodeficiency syndrome (AIDS) is firmly established"—citing only the three "discovery" papers published, respectively, by Montagnier in 1983, Gallo in 1984, and Levy in 1984.
Expressions of doubt or skepticism—let alone support for other hypotheses—were extraordinarily rare throghout this period from 1984 to 1986. The Lancet 's initial editorials reporting on the Heckler press conference and on Gallo's articles in Science criticized the public fanfare and argued for a sober assessment of the facts. The journal noted that the finding of a virus "is no proof of causality," given the possibility "that these viruses are simply passengers—yet another opportunistic infection to which these patients are susceptible." "Nevertheless," the editorial went on to say, the fact that two laboratories had isolated the viruses from AIDS patients and that the viruses had been identified in many of the risk groups and rarely in controls "[lends] credence to our prejudice that viruses such as these are likely to be the guilty party."
One article in the New England Journal , published in August 1984, noted in passing that "further evidence is necessary to substantiate [the] possibility" of a retroviral cause. More serious doubts tended to be voiced only in short letters to journals. Arthur Ammann of UCSF Medical School called for a "cautious appraisal" in a September 1984 letter to JAMA . Arguing that "there is no historical precedent for believing that a single infectious agent is capable of abolishing a normal immune system," Ammann suggested that AIDS might conceivably be
the consequence of "multiple infections" involving HTLV-III acting synergistically with other viruses, such as CMV. Before concluding that HTLV-III is the sole cause, he cautioned, "a great deal more evidence must be obtained." But interventions such as these failed to gather any allies, and they largely vanished from the pages of the prominent medical and scientific journals after 1984.
What role did Gallo play in pushing the argument that his virus was the cause of AIDS? Articles authored or coauthored by Gallo or his coauthors certainly accounted for a substantial part of this literature—about a third of all publications in the sample for 1984 and 1985 and a quarter of them for 1986. (Of course, in many of these cases where the names of Gallo and/or his coauthors appear somewhere in the middle of a lengthy list, Gallo's lab most likely played a marginal role, perhaps no more than supplying viral samples.) But an interesting finding, revealed in table 2, is that, in terms of the pattern of making qualified or unqualified claims, there are no statistically significant differences between the papers influenced by Gallo's group and those with other authorship. As Treichler has asserted, Gallo's group may have strengthened the credibility of their claim simply by publishing so many papers about AIDS and referencing their 1984 paper at every turn. But in referencing it, they were no more or less likely to make either qualified or unqualified etiological claims than other scientific researchers who cited it during the same years. They promoted their product—but they did not, in any crude or blatant sense, oversell it in terms of its causal implications.
On the other hand, Gallo and his collaborators were less circumspect than Montagnier's group, who, as late as March 1985, wrote cautiously in JAMA: "Although the precise role of LAV in the pathogenesis of AIDS remains to be confirmed, the present report, together with the recent description of HTLV-III and AIDS-related virus, provides growing evidence in favor of a T-lymphotropic retrovirus as the causative agent in AIDS." And in November 1985, Montagnier reminded his readers that "cofactors"—factors in addition to the primary cause, such as antigens or foreign proteins—might often work together with LAV to cause AIDS. Montagnier, in other words, sought to incorporate some of the claims contained in earlier hypotheses, such as the immune overload hypothesis, within a new explanation that gave star billing to LAV.
A remarkable aspect of the change that took place over the three-year period is that the trend is observable even among those papers that
do not cite any subsequent research. Table 3 shows all papers in the sample from 1985 and 1986 that made a causal claim when citing Gallo's paper (as opposed to citing him for some other reason). These papers (ninety in 1985 and sixty-nine in 1986) are divided into two groups: those that cited Gallo alone or Gallo in conjunction with other previous or roughly contemporaneous "discovery" papers, such as work by Montagnier and Levy; and those that cited Gallo in conjunction with at least some later research. One might expect that papers also citing later research would be more likely to make unqualified claims. While that apparently is not the case in 1985, it seems to be in 1986. (The numbers are too small for the results to be statistically significant, but twelve of fourteen such articles made unqualified claims.) However, two points deserve note. First, only a minority of
the articles that made unqualified claims about the virus being the cause (five out of twenty-six in 1985 and twelve out of forty-nine in 1986) pointed to any later research when making such claims. In both years, most articles that made unqualified claims referenced the early set of papers only. Second, even among those articles that failed to cite any subsequent research, the original trend is apparent: between 1985 and 1986 the ratio of qualified to unqualified claims shifts markedly. These articles would seem to follow Gallo's own lead, gradually reinterpreting the significance of the early papers by imputing to them a stronger causal claim than even their authors made at the time of their publication.
To be sure, one might argue that people who failed to cite the subsequent research have been influenced by it nonetheless. Perhaps when researchers cited the early papers as having "proven" that HIV causes AIDS, they intended these citations to serve as a kind of shorthand or synecdoche that symbolically represented the larger body of published scientific literature. For this reason alone, it makes sense to attend to the other research findings published in this time period that supported the HIV hypothesis. However, many of the subsequent articles
that were co-cited with Gallo's provide little additional evidence. The two most commonly cited articles (each cited three times by articles in the sample making unqualified claims)—Samuel Broder and Gallo, published in the New England Journal in November 1984, and Flossie Wong-Staal and Gallo, published in Nature in October 1985 —are review articles summarizing the literature on the "HTLV family" of viruses. The only additional etiological evidence that Broder and Gallo provided appeared in a brief mention of unpublished data from Gallo's lab showing (1) that HTLV-III had been found in semen and saliva in addition to blood, and (2) that HTLV-III had, by this point, been isolated from over 95 persons and could be recovered over 90 percent of the time from patients with "pre-AIDS." These latter data from Gallo's lab were eventually published by S. Zaki Salahuddin et al. in the Proceedings of the National Academy of Sciences , though in this paper the Gallo group also reported that they still were unable to isolate the virus from half of the patients with full-blown AIDS. The Wong-Staal and Gallo paper is essentially the same in terms of its contribution to the question of causality. The authors simply reviewed the original Science articles and the additional findings published by Salahuddin et al. in the Proceedings .
Both review articles pointed to the Salahuddin article for the new evidence, and that paper was also cited on its own by other authors in the sample. But turn to that study and the citation pathway neatly reverses direction. The authors declared that "it is clear that HTLV-III is causatively involved in the immune disorder AIDS," and they explicitly advised the reader to refer back to Broder and Gallo for a summary of the evidence. Findings such as these certainly support Treichler's claim—that Gallo and his close associates established a network of citations that served to create the impression of greater certainty than Gallo's own data warranted. In circular fashion, each article points to a different one as having provided the definitive proof; the buck stops nowhere. Still, one can find places where Gallo did a better job of summarizing the existing evidence. For example, in a less frequently cited article in the journal Blood , Wong-Staal and Gallo reviewed two types of evidence in addition to the serology studies. First, in an unpublished study from Gallo's lab, out of ten blood donors whose recipients later developed AIDS, ten tested positive for HTLV-III antibodies. Second, an "animal model" was provided when chimpanzees were deliberately infected with HTLV-III. The chimps "mounted an immune response to the virus, and some
developed enlarged lymph nodes analogous to the lymphadenopathy syndrome that often precedes AIDS." According to Wong-Staal and Gallo, these various results, accompanied by the knowledge that HTLV-III kills T cells in the test tube, "unambiguously establish HTLV-III as the etiologic agent of AIDS."
Blood and Chimps
Whether they made qualified or unqualified claims, other authors, including the Montagnier group, pointed to similar types of evidence: serology studies, transfusion studies, and chimpanzee studies. Why these types of studies? Implicitly or explicitly, researchers had Koch's postulates—or similar criteria—in the backs of their minds. Two points, if established, would greatly enhance the credibility of the HIV hypothesis: that the virus could be found in all (or some reasonable percentage of) cases of the syndrome and that the virus, when transmitted accidentally to another human or when injected deliberately into an animal, caused the same condition. Even Gallo himself, who would in subsequent years dismiss the applicability of Koch's postulates when critics complained that they were not satisfied in the case of HIV, invoked them in his paper with Wong-Staal. Describing the "unpublished observations" of ten seropositive blood donors whose recipients later developed AIDS, Wong-Staal and Gallo commented that "nature has indirectly fulfilled one of Koch's postulates by documenting transmission of the agent prior to development of the disease."
What kind of case is presented by these various studies on serology, transfusion cases, and animals? Most crucially, how do they address the alternative explanation—that HTLV-III/LAV/ARV is simply an opportunistic infection common among people with severe immunodeficiency? The serology studies were perhaps the weakest in this regard: researchers were unable to find the virus in many cases of full-blown AIDS, and they were unable to show, on the basis of blood testing, that infection preceded immunosuppression. One study by the Montagnier group presented some important data. The researchers detected LAV antibodies in seventeen of twenty-five AIDS patients, thirteen of thirteen homosexual men with "pre-AIDS," and only one of one hundred random healthy blood donors. But their innovation was to also look for antibodies in patients with immunodeficiencies that were genetically caused. Out of twenty-three such patients, none
tested positive for antibodies to LAV, "supporting the contention that LAV is unlikely to represent simply another opportunistic infection" in people who are already immunodeficient.
The chimpanzee study was subject to various interpretations. Out of three chimps injected with plasma from an AIDS patient, two developed antibodies to HTLV-III. One of them developed lymphadenopathy and a "transient decline" in the ratio of helper T cells to suppressor T cells. As of a year later, none of them had developed any opportunistic infections. Shinji Harada and coauthors, summarizing the etiologic evidence in Science , wrote with reference to this study that HTLV-III "causes a similar disease in chimpanzees"; but technically no chimp had developed AIDS (and for a decade, no chimp would). Donald Francis and his coauthors were more cautious, claiming only that the chimp study "offers the possibility of proof that LAV/HTLV-III is the cause of AIDS." "Time will show," they added, if the chimps actually develop the full syndrome.
Studies of donors and recipients of blood transfusions (or blood products used by hemophiliacs) went the furthest in confronting the question of whether the virus was the primary cause. For example, Paul Feorino and his coauthors wrote in the New England Journal in May 1985 that they had isolated HTLV-III from six transfusion recipients who had developed AIDS and from twenty two of twenty five donors who were identified as being "high-risk." In one of the six cases, both the presumed donor and the recipient had AIDS at the time the study was performed, "raising the question whether HTLV-III/LAV might represent an opportunistic infection in both." But in the other five cases, while the recipients all had AIDS, the donors were asymptomatic "carriers" of the virus. Since the donors were healthy, the virus was apparently not an opportunistic infection in their cases. And the recipients had no other known risk factors besides receipt of a tainted transfusion.
Before calling the case closed, however, one might examine an analogous study performed by prominent researchers (Harold Jaffe, Donald Francis, and others), reported in Science a month before the Heckler press conference. This group found antibodies in nine of 117 donors to twelve patients with transfusion-associated AIDS. Grouping the donors into twelve sets corresponding to the twelve patients who received their blood products, the researchers discovered that nine of the sets each included a donor who could have been the source of infection. In six of the nine sets, the antibody-positive donor fit other
epidemiological and immunological criteria as a person at risk for AIDS, and four of those six had lymphadenopathy when interviewed for the study. The irony, however, is that these scientists were not testing for antibodies to HTLV-III. They were studying HTLV-I , the virus that, in 1983, Gallo was promoting as the cause of AIDS. A month later, everyone would simply forget about HTLV-I—but the transfusion data presented in support of that virus was nearly as good as what the Feorino group would present a year later as "further evidence of the etiologic role of HTLV-III/LAV"—and Jaffe would be the second author listed on Feorino's paper.
HIV as "Obligatory Passage Point"
The Power of a Hypothesis
Why, over the course of 1984, 1985, and 1986, did AIDS researchers so overwhelmingly come to accept as given a hypothesis that—while highly plausible and consistent with many facts known about the epidemic—was not "conclusively" proven, according to the standards of evidence they claimed to support? Nothing suggests any vast conspiracy to stifle debate, though critics would later claim as much. One reasonable explanation would eventually be proposed by Gallo himself, in response to a challenge by the HIV dissenters: "As anybody in the business knows who works [with AIDS], there is more evidence that this virus causes AIDS than you have with the vast majority of diseases [that we] long ago have accepted" as caused by viruses.
Of course, it wasn't that the HIV hypothesis was problem-free. Savita Pahwa and his coauthors (who included Gallo) noted one crucial "paradox" in the Proceedings of the National Academy of Sciences in late 1985: the virus, presumed to do its dirty work by infecting and killing T cells, could be found, using "the most sensitive methods available," only in a tiny fraction of any AIDS patient's T cells—sometimes as few as one in one hundred thousand cells. An important part of the prima facie case against the virus had been its propensity to kill T cells in the test tube. But in living human beings, the virus simply could not be found in enough T cells to account straightforwardly for their disappearance in AIDS patients.
Still, the virus hypothesis had considerable evidence behind it and only a few findings seemed anomalous; no other hypothesis about AIDS had a track record anywhere nearly as impressive. What's more,
the virus gave researchers a mission. Within months of the publication of Gallo's articles in Science , other scientists began to report their findings—on the prevalence of HTLV-III/LAV antibodies in various populations, on the detection of the virus in various body fluids, on the patterns of transmission of the virus, on possible antiviral treatments, on the development of vaccines against the virus. Especially in 1984, such researchers typically were careful to make qualified claims, noting that the virus was "believed" to be the cause or was the "probable" cause. But in practice, the qualifications meant next to nothing, because the virus—and the virus alone—is what all of them were busy spending their time studying. The phrasing of one article in the New England Journal was typical: "Now that HTLV-III has been identified as the probable cause of AIDS, it is possible to confirm the modes of transmission and document the spectrum of clinical disorders caused by this agent." At last, the authors seemed to be suggesting, we all have something to do. A plausible candidate had been proposed by eminent virologists, and most researchers were content to endorse their judgment.
Clinicians, and researchers in other fields, who read the professional literature simply to keep up with the latest findings, not to critically evaluate the analyses and methodologies, were even less likely to raise questions. As Harry Collins has suggested on the basis of recent social studies of science, there is typically "a relationship between the extent to which science is seen as a producer of certainty and distance from the research front." Any fuzziness in the data that might have been observable by a trained epidemiologist or virologist was likely to be missed by the doctor treating AIDS patients, who turned to the New England Journal of Medicine just to get the bottom line.
If a scientist as eminent as Gallo had been pushing an alternative explanation, then most likely there would have been more debate and closer scrutiny of the etiological evidence. But no challenge of that sort existed. The more time passed and the more that scientists became invested in research on HIV, the clearer became the virus's social role as what Bruno Latour has called an "obligatory passage point"—a necessary way station between social actors and the satisfaction of their interests. A meeting of the Conference of State and Territorial Epidemiologists in June 1985 might be singled out as the defining moment that the HIV hypothesis became a social fact. Conference members approved a series of resolutions, adopted soon afterward by the CDC, that redefined "AIDS" to make diagnosis dependent on a positive
antibody test result along with the presence of any one of an expanded list of opportunistic infections and cancers. People whose antibody test came back negative would in most cases be diagnosed as AIDS-free, even if they, too, suffered from one of the conditions on the list.
Those who did challenge the hegemonic position risked strong resistance and career repercussions. The story of Shyh-Ching Lo, a young virologist at the Armed Forces Institute of Pathology, is instructive in this regard. When in 1986 he reported finding a "novel virus" in tumor cells taken from AIDS patients with Kaposi's sarcoma, Lo "brought a heap of abuse down on his head," in the words of a reporter for Science . Lawrence Altman treated the story as important, and the Times gave it front-page treatment. But skeptical AIDS researchers, including Gallo, lashed out at Lo, claiming he had failed to justify his claims. Lo pressed on, discovering the agent in various body tissues of AIDS patients; when he injected it into four silverleaf monkeys, they all died within nine months. Furthermore, Lo was able to isolate the agent from six HIV-negative patients who had symptoms similar to those of AIDS. Yet his articles were rejected by more than half a dozen journals before finally seeing the light of day in the American Journal of Tropical Medicine and Hygiene in 1989.
Eventually, it became apparent that the agent Lo had isolated was not a virus but a primitive organism called a mycoplasma. Since mycoplasmas are common contaminants of tissue cultures, it remained debatable whether the mycoplasma had really come from the AIDS patients. But only in 1990, when Montagnier independently began talking about a possible role for mycoplasmas as a cofactor in AIDS, did researchers belatedly begin to take Lo seriously. Until that time, Lo—despite his credentials as a virologist—could not make his voice heard over the chorus supporting the reigning theory.
Science, the Media, and the Construction of Social Reality
What cannot be overstated is that the HIV hypothesis was not simply a scientific powerhouse. It was also—crucially—a social phenomenon. Immediately after the discovery of the probable cause of AIDS was announced, the hypothesis began its work of transforming the world and reshaping people's lives. Within two years, the first patients began taking azidothymidine (AZT), an antiretroviral drug that—at least temporarily—prevented the virus from replicating;
prescribed for many thousands of patients, AZT has earned millions of dollars for its manufacturer, Burroughs Wellcome. Even before that, thousands of people were touched irrevocably by the machinery of antibody testing, which sorted them into polar categories of "positive" and "negative." Gay communities were quite simply split into two groups; and despite frequent and sincere criticism of the tendency, antibody status became a decisive marker of identity—the sort of attribute gay men mentioned in personal ads, along with skin color and sexual predilections, to describe who they were and who they sought. In response to a belief in the HIV hypothesis, thousands of people changed the way they had sex—supposedly one of the most intractable aspects of human behavior. Even a practice as thoroughly unthinkable, in the contemporary U.S. political context, as providing intravenous drug users with clean needles suddenly became a reasonable, if controversial, health strategy that sane politicians might propose or endorse. Within a few years, the HIV hypothesis quite simply restructured the world, altering what millions of people did and said.
The mass media both mirrored and facilitated the process by which HIV became a social fact. A content analysis of selected articles from the New York Times suggests the trend over the period from 1984 to 1986. (I examined all twenty-one articles published in the latter half of 1984 that discussed both AIDS and the virus; in 1985 and 1986 news coverage skyrocketed, and I examined every fifth such article, in chronological order: forty-three articles in 1985 and fifty-one in 1986. )
In the second half of 1984, articles that discussed both AIDS and the virus were cautious in their conclusions (see table 4). Out of twenty-one such articles, eighteen made only qualified claims about the virus as the cause. By 1985, a striking shift had occurred: Out of forty-three articles in the sample for the year, twelve made only qualified causal claims and eight made only unqualified claims. Seventeen articles (41 percent) made no explicit claims yet clearly conveyed their implicit endorsement—in sixteen of seventeen cases by the unqualified use of the phrase "the AIDS virus" in reference to HIV. By 1986, the number of articles making only qualified claims had dropped to five out of fifty-one; ten articles made only unqualified claims; and the number of implicit claims rose to thirty-three (65 percent of the total). The decline in the use of qualifiers and the growing reliance on phrases such as "the AIDS virus" (or, more problematically, "the AIDS test") tell a clear story: reporters took for granted that the cause of AIDS was known. They had their doubts, to be sure, about whether Gallo
was the one who should receive credit for discovering it, but that the virus was indeed the cause was only very rarely questioned.
Articles in the Times in mid-1984, such as one by Judy Glass on June 3, discussed the reports of a viral cause in tentative terms. Glass quoted a medical professor who asked whether the virus was "the chicken or the egg"—the real cause or just another opportunistic infection. In October, Lawrence Altman sounded a more definitive note: researchers had "taken a major step toward fulfilling Koch's postulates" by transmitting the virus to chimpanzees. From about that time onward, articles by Altman—the Times 's main authority on AIDS—stopped expressing any doubts. In the second half of 1984, Altman wrote six articles about AIDS and the virus which made only qualified claims about its causal role and one that made both unqualified and qualified claims. In 1986, out of the seven articles in the sample that were by Altman, none made any qualifications. Two made unqualified claims only, while five simply implied that the virus was the cause (in four cases by referring to HIV as "the AIDS virus"). Altman did, however, write articles that discussed some of the anomalies in the HIV hypothesis, such as the mystery of why so few T cells appeared to be infected with the virus.
The Appeal of a Virus
Elsewhere in society, the viral hypothesis found a ready audience. Gay communities in general and AIDS organizations in particular were little inclined to dispute the causal role of HIV. As early as December 1984, in an information packet distributed to local health care providers, the San Francisco AIDS Foundation made its views plain: "A multiplicity of theories concerning AIDS causation has given way in most quarters to the conclusion that a specific retrovirus is the causative agent." More often, as Dennis Altman has pointed out, politically liberal groups have tended to endorse environmental, multicausal models of illness and to criticize the "single bullet" approach. In this case, however, AIDS organizers had good reason to find the HIV hypothesis attractive. Increasingly, gay men had been under attack, accused by various right-wing spokespersons of pursuing a "promiscuous" lifestyle that was in reality a "deathstyle." Fears that they would be quarantined en masse had become widespread among gays. Indeed, Dr. Edward Brandt, Reagan's assistant secretary of health in 1983, has since indicated that the Reagan administration gave serious consideration to the idea of a mass quarantine
at that time. But while the talk about lifestyle had seemed to lay the groundwork for victim blaming in the larger society, the viral hypothesis had more neutral moral implications. Pursuing a lifestyle was seen as a choice; contracting a virus seemed more like plain bad luck.
Not that the acceptance of the viral hypothesis served to sever altogether the popular connections between etiology and culpability. On the contrary, AIDS still was all too frequently perceived as a phenomenon whose very existence demanded a guilty party. But attention now tended to focus on the virus itself and the question of its origins. Had HIV originated in Africa, as many Western scientists maintained (to the displeasure of many Africans)? Did Cubans fighting in Angola bring the disease to Haiti? Was HIV the product of genetic engineering by the CIA or the U.S. Army, as fringe groups in the United States, along with official Soviet media sources, proposed? Had HIV or a simian form of it been unwittingly introduced into Africans via vaccines (against smallpox, malaria, or polio, depending on the theory) prepared from monkey tissue and administered in WHO vaccination programs in Africa? But while debates over these and other theories about origins of the virus raged and sometimes held various parties, nations, or continents culpable for the origins of the virus, to a significant degree they left gay men unscathed.
Furthermore, the viral hypothesis provided gay communities with an important repertoire of responses to the widespread panic over casual transmission of AIDS. Opinion polls in 1983 and 1984 suggested that large numbers of people in the United States believed that AIDS could be transmitted by coughs and handshakes, drinking glasses and shared toilet seats. Many people acknowledged that they were shunning contact with gay people against the possibility that those people might have AIDS, and gay rights groups were reporting a rise in cases of antigay discrimination in the workplace, in housing, and elsewhere in the society. Increasing knowledge about the highly specific routes of HIV infection offered a ready answer. The solution was not to avoid the risk groups , AIDS educators asserted, but to avoid the risk practices —principally, sex without a condom and the sharing of syringes. Given the near-total protection of the blood supply with the advent of the antibody tests, AIDS advocacy groups could plausibly claim that it was easy to protect oneself from getting AIDS. More radical public health measures such as quarantine were therefore unnecessary.
Finally, the viral hypothesis resonated with the "safe sex" (or "safer sex") strategies that were already being promoted in gay male communities
by 1983. Although many commentators had continued to stress the importance of limiting the number of sexual partners, others had focused on a different solution: taking standard steps to prevent the spread of sexually transmitted diseases, such as using condoms or avoiding ejaculation inside the body. Michael Callen and Richard Berkowitz had emphasized these points in a forty-page booklet, "How to Have Sex in an Epidemic," that enjoyed considerable circulation in gay communities on both coasts.
Given evidence that HIV could indeed be blocked by condom use, the viral hypothesis solidified a "sex-positive" AIDS education strategy. While mainstream public health officials continued to counsel monogamy, the fledgling grassroots AIDS organizations put forward a different message that was both pragmatic and scientifically based: have as much sex as you like, as often as you like, with as many different people as you like, and as long as you follow a set of rules to prevent the transmission of HIV, you will be (almost entirely) safe. (Monogamy, by contrast, was a far less credible prevention measure, the grassroots AIDS educators pointed out: especially in communities where HIV was prevalent, monogamous unsafe sex might be quite dangerous, while monogamy in the context of safe sex was essentially redundant.)
Despite frequent opposition from government funders concerned about sexually explicit language and images, the grassroots AIDS educators set out to "eroticize" safe sex—to make it seem not only normative behavior, but attractive and sexy. Techniques of safe-sex education and even the precise definitions of safe sex became, in effect, a "zone of control" that emerging community-based organizations carved out of the larger terrain of the viral hypothesis. That they were experts on safe sex was acknowledged early on: in the midst of the 1984 controversy over whether to close down the gay bathhouses in San Francisco, a state superior court judge who heard arguments on the case mandated that the San Francisco AIDS Foundation would define which activities practiced in bathhouses were safe and which were not. Yet to a significant extent, assumptions of their expertise came to depend on the widespread acceptance of claims about HIV transmission and its causal role in AIDS. Without the belief in HIV as the cause, AIDS organizers could have continued to promote their safe sex guidelines, but only as plausible measures that seemed likely to work. With HIV, the idea of safe sex rested on the shoulders of scientific authority.
Certainly dissenting voices spoke out, and more so in the gay and lesbian press than anywhere else. The Advocate , the most mainstream of the major news sources on AIDS, was the least critical of researchers. Nathan Fain, the magazine's health writer, considered the question of causality closed after the reports of the chimpanzee studies. "What all this means to the man and woman on the street," wrote Fain, "is that … convincing proof now exists that there is one virus that is the sole triggering mechanism of AIDS." Cofactors might also be necessary to cause the full syndrome, but—as the headline put it—"The Proof Is In on a Virus."
GCN , more inclined toward suspicion of experts and no friend of Robert Gallo's, took a more cautious position. Christine Guilfoy, one of the chief writers on the topic, referred to the causal claim in qualified terms throughout 1984 and 1985. A year after the Heckler press conference, in April 1985, Guilfoy wrote: "Although many believe HTLV-III plays a primary role in the development of AIDS, it is still unresolved how the virus works and what cofactors, if any, play a role." Particularly by the second half of 1985, however, writers in GCN tended to refer to HTLV-III without further explanation of its relationship to AIDS. It was simply assumed that the reader understood what this virus was and why it was being written about. Of course, referring to HTLV-III carried different implications than speaking of "the AIDS virus," as mainstream reporters were apt to do. Like the gay press generally, GCN avoided (and often criticized) the phrase "AIDS virus" for its implied conflation of two states: seropositivity and illness from AIDS.
GCN was also a place where alternative views could gain expression. In late 1986, John Lauritsen, a survey researcher and writer who had coauthored a pamphlet warning gay men about the dangers of poppers, raised the question of whether HIV had definitively been proven to cause AIDS: "Notwithstanding the thousands of assertions that have appeared in the popular media and in government press releases, the fact remains that medical science has a series of tests that any microbe must pass before it can be considered the cause of a particular disease. These tests are known as 'Koch's Postulates,' and the 'AIDS virus' has soundly flunked them." Concluding that HIV cannot be the cause of AIDS, Lauritsen reopened an old can of worms: "There must be something in the gay lifestyle that is causing gay men
to develop AIDS." Consistent with his earlier focus on poppers, Lauritsen targeted "the 'recreational drugs' … that became a prominent feature of the urban gay male lifestyle beginning in the early 1970s."
The true voice of dissent, however, was the New York Native , for which Lauritsen most regularly wrote. Indeed, the Native and its publisher Chuck Ortleb increasingly located themselves on the fringes of the emerging AIDS movement, precisely through their incessant skepticism (some would claim, paranoid doubt) about the HIV hypothesis. Writing in the Native in fall 1994, Joseph Sonnabend, proponent of the immune overload hypothesis, advised gay men not to read too much into the HTLV-III antibody test: "It should be emphasized at this point that the question of whether HTLV-III plays any role in the pathogenesis of AIDS must remain open." The following year, Sonnabend expanded on his views in an interview in the Native , speculating about the motivations and interests behind the emphasis on HTLV-III as the sole cause of AIDS and questioning the certainty of expert pronouncements: "Unlike what Dr. Anthony Fauci and Dr. Robert Gallo tell us, we are very far from understanding this disease. Very little is known. The sort of smugness that emanates from the government scientists is offensive, considering what is at stake.…"
The Native treated Sonnabend respectfully as its resident authority, but when it was Gallo's turn to be interviewed, he had no such luck. In August 1984, James D'Eramo tried to corner Gallo on the question of whether HTLV-III had been proven to be the sole cause of AIDS:
[D'Eramo :] What about fulfilling Koch's postulates …?
[Gallo :] … Koch did not fulfill those postulates in much of the work he did. They're hardly ever fulfilled in viral and fungal diseases, and hardly ever in parasitic diseases.… What's the remaining part of Koch's postulate that is not fulfilled anyway?
[D'Eramo :] It's the animal model.
[Gallo :] … you don't need an animal model in immunological diseases. Those of us who know a little bit about retroviruses realize that in some retroviruses you can't go outside the species to reproduce the disease.
In frustration at D'Eramo's questioning of the causal claim, Gallo finally challenged him directly, asking, "Why does anyone resist this data?" Gallo continued: "All I can say is that they don't know the data, they don't understand it, or they may not know some of the data
that aren't published yet. Nobody at high levels in science is arguing about this data." Often outspoken, Gallo probably never considered the impact of his tone on readers of the Native or on its staff. Nothing could have been better calculated to offend the sensibilities of the Native and inflame its constituency than Gallo's implication that the scientific debates were over the heads of laypeople, who should rest content to leave it up to the experts.
Meanwhile, the Native committed itself to a range of rival theories about the causes of AIDS. The process had its origins back in 1983, when the newspaper began promoting the view that AIDS was linked to an epidemic disease in pigs, called swine fever. This hypothesis was first floated by a postdoctoral fellow at the Harvard School of Public Health, named Jane Teas. In a 1983 letter to Lancet , Teas proposed that AIDS might be caused by a variant of the African Swine Fever Virus (ASFV), which had never been known to infect humans. Teas had done no research on AIDS or swine fever, but she was struck by the apparent similarity in symptoms as well as by the Haitian connection: AIDS seemed to have appeared in Haiti in 1978 and swine fever in 1979. She speculated: "Perhaps an infected pig was killed and eaten either as uncooked or undercooked meat. One of the people eating the meat who was both immunocompromised and homosexual would be the pivotal point, allowing for the disease to spread to the vacationing 'gay' tourists in Haiti."
In 1983, at a time when the question of etiology was still open, Teas's letter prompted some response. Two groups of researchers, one Haitian, the other Belgian and Dutch, wrote letters to Lancet saying they had looked for antibodies to ASFV in small samples of AIDS patients but with negative results in all cases. Later the 1984 AMA review article on AIDS would acknowledge the swine fever hypothesis as one of many legitimate ideas that simply failed to pan out. Teas, however, felt that the responses to her hypothesis were inadequate, and she became convinced that the scientific establishment was shutting her out. She had written to both the CDC and the U.S. Department of Agriculture, but received no "satisfactory" response from either organization. When Chuck Ortleb, the Native 's publisher, approached her, she was happy to promote her ideas and to voice concern about the "hostility" and closed-mindedness of government science.
Teas was the sort of person who would have minimal credibility in mainstream scientific circles—after all, she casually admitted that she
began "knowing nothing about AIDS" and that she taught herself about swine fever in an afternoon's reading. But to Ortleb, this kind of self-education by nonexperts epitomized the critical attitude toward scientific authority that he had been promoting in the pages of his newspaper. Through a series of articles, Ortleb pushed the swine fever angle, asking why government researchers were so slow to follow it up and insinuating that the government was acting at the behest of the pork industry.
In a striking demonstration of the perceived importance of the gay press in the eyes of the public health officialdom, James Mason, the conservative Mormon director of the CDC, flew to New York in early 1984 to try to reason with the Native 's publisher. Mason even gave Ortleb a scoop—two weeks before he spoke with the New York Times —about LAV being the probable cause of AIDS. But Ortleb became convinced that Mason was trying to divert his attention and "co-opt" him, and though the Native began reporting on LAV and HTLV-III, the newspaper also continued to promote Ortleb's pet theory.
Ortleb's single-handed campaign eventually succeeded in inducing New York State health authorities to search for ASFV in AIDS patients and in generating some coverage of the hypothesis in more mainstream newspapers such as the New York Times . But when further supportive evidence of a causal role for ASFV was not forthcoming, Ortleb was on to the next rival theory, and then the next—Lo's mycoplasma, Duesberg's heretical views, and in recent years the claim that AIDS and chronic fatigue syndrome are different forms of the same disease. Over time, the Native 's star began to fall, and Ortleb became an increasingly controversial figure within the AIDS movement. Cultural critic and AIDS activist Douglas Crimp complained in 1987: "Rather than performing a political analysis of the ideology of science, Ortleb merely touts the crackpot theory of the week, championing whoever is the latest outcast from the world of academic and government research."
Markers of Credibility
Despite speculation about swine fever and mycoplasma, despite challenges from people like Lauritsen and Ortleb, and despite some scientific interest in cofactors, the basic fact remained: The proposition "HIV causes AIDS" was hegemonic in U.S. science and society as 1986 came to a close. That year, the American Medical Association
had published in book form an authoritative collection of articles on AIDS that had appeared in recent years in its journal, JAMA . Although the collection included the Sonnabend, Witkin, and Purtilo article from 1983 (buried near the end in a "Special Reports" section), it contained no articles published later than 1983 that questioned the relationship between HIV and AIDS. For the back of the book, the AMA's Task Force on AIDS had reviewed "the complete list of published articles" on AIDS in the medical and scientific literature, with the goal of preparing "a brief bibliography that could serve as a source document to guide the interested reader through the massive body of literature on AIDS." The section on etiology contained fifty-six references, of which fifty-four alluded to a retroviral cause of AIDS in the title. Only one of the fifty-six articles proposed an alternative etiology—an article by J. J. Goedert on the role of recreational drugs in causing AIDS. Even the Sonnabend, Witkin, and Purtilo article—included in the collection itself—failed to make it into this definitive bibliography.
Another important benchmark of the credibility of the HIV hypothesis was the influential Confronting AIDS , a survey of knowledge and a blueprint for action published by the National Academy of Sciences' Institute of Medicine. Prepared by a blue-ribbon panel consisting of prominent virologists, clinicians, public health experts, and social scientists, the 352-page report encapsulated the official, credible body of knowledge about AIDS circa 1986. Though ostensibly a study of "the AIDS epidemic," the report might more accurately be called "Confronting HIV "; early in the introduction, it explained that "AIDS" is only a surveillance definition used for epidemiological purposes and that the term "does not include the full spectrum of conditions now known to be associated with HIV infection."
Nonetheless, in a section entitled "The Causative Agent of AIDS," the report did briefly review the growing evidence that HIV caused the syndrome. First, antibodies reactive to viral proteins were found in "nearly all instances" of people with AIDS, while tests of people not in "high-risk" populations were "uniformly negative." Moreover, the prevalence of antibodies in different groups corresponded with what was known about the geography and timing of the epidemic. Second, the virus itself could be isolated from the white blood cells of most people who were antibody positive; the authors added parenthetically that "the failure to isolate the virus from all infected persons is most likely due to technical limitations in the lymphocyte
culture methods and to the depletion of target cells in the advanced stages of the disease." Finally, the blood transfusion data were compelling: they "clearly showed that the virus could be transmitted to a previously uninfected person who could then develop AIDS.…"
Elsewhere in the report, however, the authors acknowledged a good deal of uncertainty. They noted that it remained mysterious precisely how HIV caused the characteristic depletion of T cells, given the small percentage of cells that appeared to be infected. This was a problem but not an insoluble one, the report implied, noting that many researchers had begun speculating about the "indirect" means by which HIV could be causing T-cell loss. Montagnier, for example, had proposed that HIV initiated an autoimmune mechanism, whereby the immune system of the infected person was "fooled" into killing its own T cells; and other hypotheses were equally complex.
Another question was whether HIV worked alone to cause AIDS or whether some "cofactor" or "cofactors" might also be involved. But despite raising these various questions about how HIV caused disease and whether HIV worked alone, the main thrust of the report was to focus squarely on the problem of HIV infection. Thus chapter 6 of the report, "Future Research Needs," divided research priorities into the following categories: structure and replication of HIV, natural history of HIV infection, epidemiology of HIV infection, animal models for HIV infection, antiviral agents, vaccines against HIV, and social science research.
John Lauritsen, who titled his review of Confronting AIDS in the Native "Caveat Emptor," noted: "For those who are true believers in the 'AIDS virus' ideology, a number of disconcerting bombshells are detonated in this book. To begin with, the report acknowledges that it is impossible to isolate HIV from many AIDS patients and that some AIDS patients show no evidence of ever having been infected with the virus." Yet as Lauritsen was no doubt painfully aware, the "bombshells" simply failed to echo in the larger society or even in the sectors of it that concerned themselves principally with the epidemic. In a few short years, an industry had grown up around AIDS, encompassing doctors and researchers, service providers and grassroots educators, lawyers and writers, politicians and policymakers—a complex of individuals, groups, and formal organizations. And within this industry, HIV was the common link between actors and interests. The virus was the "obligatory passage point" that stood between people and the
grants they sought to obtain, the programs they endeavored to establish, and the propositions they wanted to advance. In its transformation into scientific fact and social reality, "HIV causes AIDS" had become a "black box"; and when people like Sonnabend or Lauritsen tried to reopen the box and review the evidence and arguments, theirs were isolated voices with minimal credibility. It would take someone with considerably more scientific capital to focus significant scientific and extrascientific attention on the question of whether HIV had in fact been proven to cause AIDS.
Reopening The Causation Controversy
From Deafening Silence to the Pages of Science (1987–1988)
How does a controversy that seemed to have been closed come to be reopened? What sort of tactics enable someone to disrupt the smooth transfer of knowledge from hypothesis to fact to common sense? The story of Peter Duesberg, who became the premier "HIV dissenter," is an enlightening one. Like other prominent researchers, Peter Duesberg proceeded to AIDS from prior work on retroviruses and their relation to cancer. Born in Germany in 1936, Duesberg received a Ph.D. in biochemistry from the University of Frankfurt; in 1970, he joined the faculty of the University of California at Berkeley in the Department of Molecular and Cell Biology.
In the 1970s, as millions of dollars were poured into the "War on Cancer," cancer research increasingly came to be dominated by what Joan Fujimura has called the "bandwagon" of oncogene theory. This theory held that certain genes within each cell had the potential to cause cancer. Closely tied to oncogenes were the cancer-causing retroviruses, which, it was argued, contained genes that could turn normal cells into cancer cells. Duesberg not only mapped the genetic structure of retroviruses but was the codiscoverer of the first known
oncogene, called src (pronounced "sark"). These accomplishments established him as a figure of note in his field.
To date, Duesberg has authored or coauthored more than 200 professional publications. A survey of the "Medline" database, which lists scientific publications that are medically relevant, shows more than 150 articles, literature reviews, monographs, and letters authored or coauthored by Duesberg. A study of the Science Citation Index , a crude but not uninformative indicator of a scientist's perceived importance in the eyes of peers, reveals that publications with Duesberg as first author have been frequently cited over the years, though particularly in the late 1970s. Between 1975 and 1979, for example, 76 of his publications were cited more than one thousand times. By comparison, during the same period, publications by his contemporary and colleague, Robert Gallo (that is, those with Gallo as first author), received over eight hundred citations. These figures put both scientists in the exceptional category, since articles listed in the Science Citation Index are cited on average only a handful of times a year—indeed, many are not cited at all.
Over the course of his career, Duesberg has received a number of awards and prizes, including being named the 1971 California Scientist of the Year. In 1986, the NIH awarded him an Outstanding Investigator Award, a special research grant for high achievers. In April of that same year Duesberg was elected into the National Academy of Sciences (NAS)—the cream of the crop, numbering about fifteen hundred of the top scientists in the United States. But Duesberg's career has not been without controversy. Indeed, in recent years, he had increasingly positioned himself as somewhat of a maverick, challenging the same conventional wisdom that he had earlier helped to construct. By the mid-1980s, Duesberg had become known as a dissenter from oncogene theory. "We have this nice idea of the oncogene model as some kind of switch" that turns on cancer, Duesberg told Forbes magazine, "but it has yet to be proved." In 1985 Duesberg published a formal challenge to oncogene theory in Science . Not everyone accepted Duesberg's argument, but neither did Duesberg suffer professional consequences as a result of his heterodox position. Indeed, both his Outstanding Investigator Grant and his induction into the NAS followed on the heels of his dissent.
Posing the Challenge
In many respects, the concerns Duesberg expressed in his article in Cancer Research , published in March 1987, were an extension of those he had voiced earlier. Entitled "Retroviruses as Carcinogens and Pathogens: Expectations and Reality," this sixteen-page review article with 278 references presented no original research but continued the argument that Duesberg had been trying to put forward: that retroviruses are simply not "the vessels of evil they have been labeled to be." In recent years, the general hypothesis that viruses were linked to cancer had been gaining ground, in part because many viruses (both retroviruses and ordinary DNA viruses) had been isolated from tumors and leukemias, particularly in animals. Duesberg pointed out, however, that many of these same viruses "were subsequently found to be widespread in healthy animals and humans." In his view, only a specific subset of these viruses were actually oncogenic (cancer-causing): those containing a class of genes called onc genes. Retroviruses lacking these onc genes, according to Duesberg, were harmless and ubiquitous; they could "coexist with their hosts without causing any pathogenic symptoms."
Without question, had Duesberg stopped there his article would have been ignored by everyone outside of a narrow specialist community. But Duesberg had another point to make, one that would occupy the final third of the article. The scientist later recalled: "As I was writing … AIDS just sort of literally exploded into the news media, and an article on retroviruses not at least taking a position [on] AIDS would have been rather incomplete. …" From Duesberg's perspective, the identification of the HIV retrovirus as the causal agent in AIDS was highly problematic. First, he pointed to the considerable disparity between the number of people estimated to be infected with HIV and the number of people who actually had AIDS. In the United States, where one to two million people were believed to be HIV positive, the annual incidence of AIDS among the virus-infected groups was only 0.3 percent. In Haiti and Africa, where estimates of infection ran even higher, the annual incidence was estimated at less than 0.01 percent. Since the introduction of the hypothesized agent so rarely appeared to cause disease, Duesberg claimed that Koch's third postulate had not been satisfied.
Second, Duesberg argued that it was implausible that a retrovirus would cause illness years after infection. He noted that many people
infected with HIV report having a brief, mononucleosis-like illness a few weeks after infection, and that this is what might reasonably be expected from a retrovirus. By contrast, the claim that HIV also caused AIDS some years later was hard to reconcile with the claim that HIV directly killed T cells: "We are faced with two bizarre options: Either 5 year old T cells die 5 years after infection or the offspring of originally infected T cells die in their 50th generation, assuming a generation time of one month for an average T cell." Furthermore, Duesberg noted that, in a study published in 1986 and conducted by Gallo and his associates, viral RNA was detected in only one of every ten thousand to one hundred thousand T cells in infected persons. In Duesberg's view, it was absurd to claim that a virus expressing itself in so few cells could be causing so much damage, since the body is constantly manufacturing new T cells. Even if the virus were to kill every ten-thousandth T cell every twenty-four hours, "it would hardly ever match or beat the natural rate of T-cell regeneration." Finally, Duesberg argued that there was no "simian model" for AIDS as required by a strict interpretation of Koch's postulates. Studies of chimpanzees and monkeys deliberately infected with HIV showed that these primates failed to develop a condition like AIDS (although such primates did develop viral antibodies, along with a mononucleosis syndrome similar to that in humans, shortly after infection).
What, then, did it mean to test HIV antibody positive? For Duesberg, it meant that one was protected against the effects of HIV: The purpose of antibodies is precisely to protect the body against the spread and expression of a pathogen. Having antibodies to HIV was therefore like being vaccinated against the virus. Until the immune system had created these antibodies, the person infected with HIV might suffer from the mononucleosis syndrome; but once the person tested positive for antibodies (normally within weeks after infection), he or she was safe—at least from HIV. HIV didn't harm its hosts; it was simply one of the many viral infections sustained by people with AIDS or at risk for AIDS, as was Epstein-Barr virus and CMV (found in 80 to 90 percent of them) and herpes (found in at least 75 percent). Perhaps AIDS was caused by one of these other infectious agents, perhaps it was caused by something other than a virus; Duesberg had no way of knowing. But HIV alone "is not sufficient to cause AIDS and … there is no evidence, besides its presence in a latent form, that it is necessary for AIDS."
A Controversy Takes Public Shape
Most scientific publications, sociologists of science have pointed out, are destined to die a lonely death. Given the tremendous number of publications that appear each year, it is inevitable that the average paper is ignored by the vast majority of scientists. Only a minority of papers are cited by many others; fewer still become the object of direct debate. As a general rule, one need not invoke a complicated explanatory apparatus to account for the fact that a scientific paper may sink beneath the surface of professional attention without causing much of a splash.
Duesberg's paper might have been particularly inclined in that direction because many of the points he was making were not especially new. Such questions as how the virus could cause the near-elimination of T-cells when only a few seemed to be infected had been raised before; this particular anomaly had made it into the National Academy of Sciences' Confronting AIDS and had even been discussed in the gay press. But arguably Duesberg's essay was different, and it might have been expected to generate a livelier response. It was written by an eminent scientist whose articles typically had been cited by dozens of other scientists each year. It was published in a respected journal. It had enormous implications if correct in its arguments. And it constituted nothing short of a declaration of war on some of the most prominent virologists in the world. Yet had it not been for the pressure exerted by outsiders who wrote about Duesberg in the alternative and mainstream press, the scientific community might never have addressed Duesberg's claims. Indeed, throughout the latter part of 1987 and early 1988, it was precisely the "AIDS establishment's" apparent avoidance that most incensed the HIV dissenters—and that provided them with their best ammunition.
The first apparent published mention of Duesberg's article came in a cover story by John Lauritsen in the June 1, 1987, issue of the New York Native . As the issue's cover advertised, the focus of the article was to encourage people with AIDS not to take the medication AZT. Recently approved for AIDS patients, AZT was believed to inhibit replication of the virus in infected cells by interfering with the process of reverse transcription. AZT, in other words, made sense as a treatment for AIDS only if AIDS was caused by HIV. This is precisely what Lauritsen disputed, and much of the article was devoted to the proposition that "HIV Is Not the Cause of AIDS."
With the discovery of the virus, "dogma rapidly came to prevail"; "all other research efforts were shunted aside, ostracized, under-funded," Lauritsen complained. Against this dogmatism, it was—until now—impossible for dissenters to make their voices heard: "Since 1984, there have been a few of us who stated in print that epidemiological evidence, together with the failure of HIV to fulfill any of Koch's postulates, made it most unlikely that HIV could be the sole cause of AIDS. … We were isolated. Some AIDS researchers did not believe in the 'AIDS virus' ideology, but, in the interests of self-preservation, they remained silent." But now that a prominent scientist had entered the fray, "all this has changed"; and the HIV dissenters could emerge from their isolation. As Latour has noted, "the power of [scientific] rhetoric is to make the dissenter feel lonely"; this is precisely what happens to the "average person" who tries to challenge highly technical scientific texts. The most obvious solution is to recruit credible allies who can provide rescue from isolation. Lauritsen had found just such an ally.
"Unless HIV's champions can do some very fancy explaining," Lauritsen concluded, "Duesberg's article has unambiguously relegated the 'AIDS virus' etiology to medical history's trash heap of falsified hypotheses." Insisting that "Gallo and the other 'AIDS virus' ideologues" must respond to Duesberg's article "fully and in detail," Lauritsen did his best to up the ante in the controversy: "If the Public Health Service and the media remain silent about Duesberg's article, and persist in expounding the discredited HIV mythology, then gay men will have cause to be gravely concerned. This would mean that the government and their confederates in the medical establishment are not acting in good faith, that nothing they say can be trusted, that their interests are hostile to ours. Their silence would raise the possibility of a horrible hidden agenda."
Soon after this article appeared, Lauritsen went to interview Duesberg at the NCI, where Duesberg was working while on sabbatical from the University of California. The interview was published both in the Native and, sometime later, in its more literary offshoot, Christopher Street; the Native ran photos of Gallo and Duesberg on its cover, with the headline "Which Man Is Right?" The interview recorded a fascinating duet between Duesberg and Lauritsen, with Duesberg voicing his support for Lauritsen's claim that AZT is poisonous ("It is a poison. It is cytotoxic.") and Lauritsen feeding Duesberg suggestions about what might cause AIDS. When Duesberg
shrugged off a direct question on causation ("Well, that's a difficult one. … I really wonder what it could be"), Lauritsen put forward the idea advanced earlier by various proponents of a multifactorial etiology that AIDS might have different causes in different groups. Duesberg chimed in: "Absolutely. And in Africa I don't think anybody knows what kind of AIDS exists, or whether AIDS exists. In the case of the drug users, I could well see that an infection of toxins—and the drugs are impure; no one knows where they come from—is hell for the immune system. And also medical injections—streptomycin or penicillin—are also not good on a regular basis. They are immunosuppressive themselves. Perhaps it is a simple question of lifestyle."
While assuring Duesberg that it was not incumbent on him to come up with an alternative hypothesis—"It's quite enough to have falsified theirs"—Lauritsen nonetheless pushed Duesberg's speculations further. He described for Duesberg what he called the "profile" of the average AIDS patient—a profile whose characteristics supposedly included long-term drug abuse, promiscuity, and repeated cases of sexually transmitted disease:
[Lauritsen: ] Looking at that profile … I think it would be surprising if such people did not become seriously sick from their lifestyle.
[Duesberg: ] I would be surprised, too. The number of contacts, the number of things they inject. You wonder how they could do it.
By the end of the interview, Duesberg appeared to be sliding out of his formal position of agnosticism and toward an endorsement of a lifestyle model similar to the immune overload hypothesis that had been so popular in the first years of the epidemic—indeed, a particularly judgmental version of that hypothesis.
According to James Kinsella's study of AIDS and the media, the Native's publisher, Chuck Ortleb, quickly took it upon himself to conduct a "phone-calling campaign" to promote Duesberg's arguments. But the Native —a paper whose fascination for unorthodox and speculative theories had left it with tarnished credibility even among its intended readership of gay men, let alone elsewhere—had only minimal power to spread the word about Duesberg or to evoke much alarm about a "horrible hidden agenda." Duesberg's claims did begin to circulate in gay communities; they were picked up, for example, by Charles Shively, writing about various alternative AIDS theories in Gay Community News . But only with Katie Leishman's September
1987 article in the popular magazine Atlantic Monthly did Peter Duesberg begin to hit the mainstream. Dubious of official pronouncements about the epidemic, Leishman's article ranged widely, exploring the possibilities of insect transmission and presenting a sympathetic portrait of Jane Teas's unappreciated efforts to push the African swine fever hypothesis. Near the end of the article, however, she also turned to Duesberg and Koch's postulates, noting that Duesberg "is so certain of his claim that he has offered to be inoculated with HIV."
Soon afterward, Duesberg made his first of what would prove to be several appearances in a British television documentary series called Dispatches . In an episode entitled "AIDS—The Unheard Voices," produced by a group called Meditel and broadcast on November 13, the narrators cited Duesberg to suggest that discrimination against anti-body positive people, however deplorable on its own terms, was particularly irrational if HIV were not even the true cause of AIDS. Though controversial in Britain, the show attracted little notice in the United States. Meanwhile, Harvey Bialy, the editor of a journal called Bio/Technology , had become interested in Duesberg's arguments, and Bialy invited Duesberg to write a summary of his Cancer Research article. Adopting a journalistic style, Duesberg complained that "the 'deadly AIDS virus' has been sold to the public as the cause of AIDS with the confidence and authority that is usually derived from absolute scientific proof."
In the immediate aftermath of the Leishman piece and Duesberg's own article in Bio/Technology , Duesberg began to be recognized in U.S. media circles as a credible and "quoteworthy" dissenter on the subject of AIDS. By the end of 1987, gay newspapers such as Gay Community News and San Francisco's Bay Area Reporter were publishing articles specifically about Duesberg—and about the failure of his colleagues to respond to him. "How come researchers continue to study HIV but have not refuted Duesberg's theory?" asked the subhead to the GCN article. "I've asked questions they apparently can't answer," Duesberg was quoted as saying.
Before long the story had acquired its own momentum. In January, Celia Farber, a journalist with the pop music magazine Spin , featured Duesberg in a long interview in her column called "AIDS: Words from the Front." In the interview, Duesberg suggested that researchers such as Gallo found themselves simply unable to retreat from their original claims because the "stakes are too high now": "Every progress report from their laboratories is discussed by Dan Rather and
Barbara Walters, Newsweek , and Time magazine. … To say that now, maybe, the antibody wasn't worth committing suicide for or burning houses for, would be very embarrassing." Even more provocatively, Duesberg delivered a stinging critique of the political economy of contemporary biomedical research, questioning the motives of AIDS researchers: "Scientists researching AIDS are much less inclined to ask scrutinizing questions about the etiology … of AIDS when they have invested huge sums of money on companies that make money on the hypothesis that HIV is the AIDS virus. … Gallo stands to make a lot of money from patent rights on this virus. His entire reputation depends on this virus. If HIV is not the cause of AIDS, there's nothing left for Gallo. If it's not a retrovirus, Gallo would become irrelevant."
As a reporter for the journal Science would later put it: "In the world of biomedical research, where ties to industry are pervasive but mentioning the fact is not, these are fighting words."
Interests, Investments, and "Fallen Angels"
Such charges made for good copy, but Duesberg's point was actually more subtle: virologists had "invested" in the HIV hypothesis—not just financially, though this was true in some cases, but personally, professionally, and psychologically. The following year, in a speech at a scientific gathering, Duesberg put forth this analysis as a full-fledged, revisionist history of retrovirology's desperate search for "clinical relevance." "On the basis of promises and expectations, the retrovirologists … have become the darlings of molecular and clinical biology in the last twenty years," Duesberg explained. Retroviruses were expected "to hold keys to cancer and other diseases," yet despite massive funding, the promise had not been fulfilled. Earlier in the century, virologists enjoyed spectacular successes against polio and smallpox. But "in the 1970's and 80's, virology suffered from the same fate that inorganic chemistry suffered in the early part of the century, when no new elements were left to be discovered!" Virology became "a thoroughly academic discipline, without significant clinical factors."
With more and more virologists at work using ever more sophisticated tools, it was inevitable that they would "succeed" in finding viruses that appeared to be linked to diseases that in fact have other causes, Duesberg argued. In this sense, virologists had become "the victims of their own weapons." Having found one such virus in AIDS
patients, virologists were now fanatically invested in the claim that the virus caused the syndrome: "An 'AIDS virus' is perhaps the last hope for the clinical relevance of the highly visible, highly decorated and powerful retrovirus establishment."
Duesberg was the first to note that it would have been simpler for him to pursue a sure thing, a "succession strategy" (to use Bourdieu's terminology), as opposed to a high-risk "subversion strategy" of scientific advancement. "Clearly the value of my very considerable investment in retroviruses would be much compounded by a clinically relevant retrovirus, which should thus motivate me to believe in HIV!" Duesberg told the gathering. "But since all work on retroviruses in the last 25 years has shown that latent retroviruses are harmless, and that virtually all retroviruses in wild animals and in humans are latent, I have lost faith in the central dogma of the program …," said Duesberg, characterizing himself as a "fallen angel, like Lucifer."
The Duesberg Story Goes Mainstream
With charges that AIDS experts were reaping millions of dollars from a discredited hypothesis, it didn't take long for the story to hit the newspapers. On January 7, the New York Post became the first daily newspaper to print an article specifically on the Duesberg controversy, called "AIDS Experts on Wrong Track: Top Doc." Writer Joe Nicholson, the Post 's medicine and science editor, cited Duesberg's offer to have himself injected with HIV, and he also quoted Gallo's protestation that "no serious scientist is interested in this." Nicholson paid considerable attention to Duesberg's credentials, noting that this "top scientist" had been studying viruses for twenty years, was a member of "the elite National Academy of Sciences," and had spend the preceding year on a scholarship at the NIH, "the world center of AIDS research." But Nicholson failed to mention that Duesberg's work at NIH was on cancer, not AIDS; nor did he justify his initial identification of his protagonist as "AIDS expert Dr. Peter Duesberg," given that Duesberg had neither conducted any laboratory research on AIDS nor had any professional contact with AIDS patients.
Perhaps predictably, the Post 's more upscale competitor was quick to follow up and to do so in a more skeptical vein. "A Solitary Dissenter Disputes Cause of AIDS," wrote the New York Times 's Philip Boffey, in a short (728-word) article published not in the front section but on the medical science page in section C. The article pitted
Duesberg's "provocative argument" against "virtually all of the leading scientists engaged in AIDS work [who] believe that Dr. Duesberg is wrong," and it quoted Anthony Fauci of NIH as saying: "The evidence that HIV causes AIDS is so overwhelming that it almost doesn't deserve discussion any more." Boffey also suggested that Duesberg's claims might be old hat: "AIDS experts insist that the issues raised by Dr. Duesberg have been considered at length within the scientific community. They cite plausible mechanisms whereby a tiny fraction of infected cells could disable vast numbers of additional cells."
A two thousand-word article by Joel Shurkin appearing soon afterward in the Los Angeles Times lent considerably more credibility to Duesberg's views. In an implicitly equalizing move, Shurkin referred to a debate between "two camps," the "dissidents" and the "AIDS Establishment," which "disagree not so much on the basis facts as on their interpretations." Shurkin's discussion of disagreement between scientists tended to convey a certain legitimacy upon Duesberg's arguments. For example, one AIDS researcher "who refused to be quoted by name" said that Duesberg was factually incorrect and that the virus had indeed been found in all patients. But another researcher "said the truth is somewhere in between." Such disagreement had the effect of suggesting that there was a legitimate spectrum of opinion on these questions and that Duesberg's views, however unpopular, were not beyond the reaches of plausible scientific theorizing.
Just as Duesberg's name was inching further into the mainstream media, Spin published a follow-up piece, an interview with Gallo in which the virologist responded—heatedly—to Duesberg's views. (William Booth, the news writer for Science , later characterized Gallo's "ranting and raving" as "bizarre," but added that the interview was tape-recorded without Gallo's knowledge. Should one keep an open mind on the question of the causation of AIDS? interviewer Anthony Liversidge, a New York City science writer, asked Gallo.
[Gallo: ] No. I don't think anybody needs to keep an open mind on that. It is silly, OK?
[Liversidge: ] Is there any flaw in [Duesberg's] logic that is easy for you to point out?
[Gallo: ] No. He's a good fellow. It's a useless interchange. Really totally useless. He's an organic chemist. I would never argue with him about electronic spin resonance in a molecule of organic compound.
Gallo went on to say, "This is just so trite that it is a waste of my goddamn time. I'm busy." Everyone knew that HIV was the cause of AIDS: "Call 5,000 scientists and ask."
Gallo's central complaint about his colleague was that Duesberg was simply not qualified to comment on the question. Or as Gallo bluntly told his interviewer: "Arguing with Peter is like you arguing with me." Furthermore, said Gallo, Duesberg had misinterpreted published evidence and ignored crucial arguments about the role of HIV in causing AIDS: "Hasn't Duesberg ever understood indirect mechanisms in cell killing? There are immune responses to the virus that destroy the proliferation of the T cell. That's crystal clear now. It is not just a matter of the virus going in and killing the cell directly. Does that take a genius?" Finally, Gallo was furious at Duesberg for failing to recognize the human consequences of his arguments: "Peter can do a lot of disservice. He has now indicated to people that they can go out and fuck around and get infected by this virus and not worry. That's the part where I am mad at Peter. Peter is joking about very serious matters that are going to alter some people's behavior."
Celia Farber capped off Liversidge's interview by appending an ironic comment, noting that a few years earlier, when Gallo introduced Duesberg at a university talk, he characterized Duesberg as having "a rare critical sense which often makes us look twice, then a third time, at a conclusion many of us believed to be foregone." And Farber quoted Duesberg's response to the Gallo interview: "I must say, of all the scientists I've known, Gallo's reactions are the most unscientific." In fact, Gallo was a convenient foil for Duesberg. Though this would change in the years to follow, at the moment Gallo was the AIDS establishment figure that everyone loved to hate. As rumors had spread that Gallo might have stolen Montagnier's virus, Gallo had come to be a symbol of expertise gone bad: untrustworthy, patronizing, and resentful of challenges. Just the past month, Gay Community News had spotlighted his attitude toward the AIDS activist group ACT UP in its "Quote of the Week" feature: "I don't care if you call it ACT UP, ACT OUT or ACT DOWN, you definitely don't have a scientific understanding of things," Gallo had reportedly told activists.
Gay Despair, Gay Suspicion
If gay men in early 1988 were apt to distrust Gallo, they were also inclined to be open to heretical views. This was a particular
moment in the history of the AIDS epidemic in gay communities, one marked both by profound desperation and the emergence of a new wave of militant activism. Gay men were wracked with frustration by the slow rate of progress in the development of treatments for AIDS, and those testing positive for HIV antibodies were increasingly pessimistic about their likelihood of avoiding illness and eventual death. Earlier on, the claim that AIDS was caused by a virus had resonated with gay concerns about avoiding discrimination and stigmatization. But this changed with reports by public health officials that the percentage of those infected with the virus who would go on to develop AIDS was not, as first believed, a small minority of 5 or 10 percent but in fact appeared to be at least 70 percent and might, in the absence of new treatments, rise as high as 100 percent. These tidings led to a deepening gloom between 1985 and 1988. For the largest and most established gay communities, where local newspapers routinely reported that one out of every two gay men probably was infected, such news can only be described as devastating. AZT at this point was prescribed only for people who already had AIDS (at a cost of about ten thousand dollars a year per person—and it was failing to keep them alive for very long). Some vocal spokespersons in gay communities, particularly in New York, argued that AZT did more harm than good. And there were no approved medications that antibody-positive people could take to keep them from progressing to an—apparently inevitable—AIDS diagnosis.
One response to these difficult times was a rebirth of activism, epitomized by the actions of groups like ACT UP and the San Francisco-based advocacy group Project Inform, that focused on eliminating the bottlenecks in the federal drug approval process, challenging the pharmaceutical houses over price-gouging for medications, and—as a popular slogan had it—getting "drugs into bodies." But a second response to the mood of desperation was a surge of interest in heretical views about AIDS. The AIDS establishment had failed to deliver; perhaps it was time to listen to some new voices. Understandably enough, cofactor theories were particularly attractive since they offered hope that not all those who were HIV antibody positive would actually develop AIDS. But more radical theories that disputed the HIV-AIDS link altogether had a certain appeal as well. Indeed, when Duesberg, along with Joan McKenna (director of an independent organization called the Institute for Thermobaric Studies, in Berkeley, and an advocate of the view that AIDS is actually a disguised form of syphilis),
was invited to speak at a public forum in San Francisco's heavily gay Castro district in January 1988, they were met by a standing-room-only crowd of six hundred. Many more were turned away at the door, according to San Francisco Chronicle reporter Randy Shilts, "reflecting the growing currency that a number of unconventional theories about the cause of AIDS are gaining in the gay community." Duesberg himself "received a hero's welcome" at the forum, in the words of an article published in the San Francisco Sentinel , a gay newsweekly.
That Duesberg should inspire the admiration of the gay masses was not without irony, given that the researcher at this point appeared to endorse the same immune overload hypothesis that, earlier in the epidemic, had often been characterized as homophobic and had been criticized for "blaming the victim." But initially people knew little about Duesberg. When interviewed by the Sentinel , Duesberg refused to give an alternative explanation for what causes AIDS, saying only, "I can't answer that." Shortly afterward, however, the Oakland Tribune quoted him as explaining: "I suspect we are dealing with an environmental lifestyle disease that has hit drug users, hemophiliacs and some gay communities the hardest. The trauma of anal intercourse could also be a factor. They could have used too many drugs, been too promiscuous, or had their immune systems weakened by venereal diseases, foreign antigens and antibiotics." More damningly, the February 2 Village Voice quoted Duesberg as saying that the epidemic was "caused by a lifestyle that was criminal twenty years ago." Days later, this remark became GCN 's "Quote of the Week."
As statements such as these became known, Duesberg lost any chance of sustaining large-scale support in gay communities. By February 1988, negative articles about Duesberg began to appear, including the Voice article, written by medical reporter Ann Fettner, called "Dealing with Duesberg: Bad Science Makes Strange Bedfellows." Duesberg's views on causation, Fettner wrote, constituted "a stunning regression to 1982, when everything under the sun, and gay practices in particular, were being blamed for the outbreak of the disease."
Yet even as Duesberg's stock was beginning to fall in gay communities, he was gaining considerable attention in the mass media and even in some government circles. On February 9, the refusal of mainstream AIDS researchers to confront Duesberg was blasted by Jack Anderson,
the syndicated columnist and well-known muckraker. According to Anderson, Harvey Bialy, the editor of Bio/Technology , had been planning a workshop called "How Does HIV Cause AIDS?" and a senior White House domestic policy analyst named Jim Warner had offered to cohost it. Warner was reported to be "frustrated about the inadequate response he had gotten to Duesberg's theory"; sponsorship by the White House "would guarantee the attendance of Gallo and other experts." Yet shortly before the conference was to take place, it was abruptly removed from the White House calendar. According to one editor at Bio/Technology , "The impression was that the pressure came from the NIH." When Anderson asked about the conference, Warner replied, "I can't talk about that." Anderson also noted that Gallo refused to return his phone calls.
The Establishment Hits Back
For the AIDS experts who thought Duesberg's arguments were pernicious nonsense, there were two choices, both of them fraught with some peril. They could continue to ignore Duesberg, at the risk of appearing closed-minded, imperious, or unscrupulous, and hope that he would eventually go away or that the media would simply lose interest. Or they could engage him directly and seek to show him up, at the risk of granting him further credibility or, at a minimum, publicity. "Many AIDS researchers refuse to comment publicly because they fear it will legitimize Duesberg," said NIH's Anthony Fauci, quoted in a March 1988 news article in Science .
Yet to many scientists, the political costs of ignoring Duesberg increasingly seemed to overshadow the risks inherent in engaging with him. Apparently in a move to undercut Duesberg's complaint of being marginalized, Dr. Frank Lilly of the Albert Einstein College of Medicine, the chairman (and the only openly gay member) of the President's Commission on the HIV Epidemic, an advisory body appointed by President Reagan the year before, responded to Duesberg's requests for an opportunity to make his views known by inviting him to testify at the commission's hearings in February. However, in what would prove to be a common theme in responses to Duesberg in the years to follow, commission members blasted Duesberg for the sin of playing to a public audience. One member, Dr. William Walsh, lectured Duesberg: "I would hope that you would press your theory within the scientific circles and not carry this uncertainty to the public.… Don't
confuse the public—don't confuse the poor people who are suffering with this disease." This appeal to Duesberg to avoid publicizing his dissent enraged Katie Leishman, who had promoted Duesberg earlier in the pages of Atlantic Monthly . She blasted the commission for its treatment of Duesberg, in an op-ed piece published in the Wall Street Journal entitled "The AIDS Debate That Isn't." Leishman reserved particular ire for Walsh: "The suggestion that the public and patients must be protected from confusion is not merely condescending but faintly sinister."
From the vantage point of the AIDS researchers and public health officials who were on the receiving end of all this criticism, the situation was rapidly getting out of hand. Into the fray stepped the American Foundation for AIDS Research (AmFAR), a prominent independent foundation that raised money for AIDS and dispensed it to a range of university-based and community-based research projects. With strong ties both to gay community representatives and mainstream researchers, AmFAR was well situated to play mediator. AmFAR sponsored a forum held at George Washington University in Washington, D.C., on April 9 and invited a range of panelists. Anthony Fauci, the most prominent government scientist present, had reservations about agreeing to participate but decided to come because "the scientific community can't afford to ignore [Duesberg] any longer."
At the forum, after Duesberg summarized what he termed the "paradoxes" of the HIV hypothesis, panelists and audience members hit back hard. Panelists insisted that Duesberg was simply wrong to say that viruses always cause disease within months and never do so in the presence of antibodies. And they noted that with the advent of a new technique for manipulating DNA called the polymerase chain reaction (PCR) it was now possible to find HIV in nearly 100 percent of samples from people with AIDS—though still not in every case, as Duesberg was quick to observe. As to the presence of HIV in so few T cells, Fauci stated that HIV also infected other immune system cells called macrophages and might hide in bone marrow cells. Fauci was particularly vehement in response to suggestions that AIDS really was linked to lifestyle: "What kind of risk behavior does the infant born of an infected mother have?" he asked. "And what about the 50-year-old woman who received a blood transfusion from an infected donor?"
Perhaps the most interesting data were presented by Warren Winkelstein, an epidemiologist from Berkeley's School of Public Health. Winkelstein's numbers came from the San Francisco Men's Health
Study, a prospective study of one thousand single men, gay and straight, twenty-five to fifty-four years old, who had been recruited by statistical sampling methods several years earlier, and who were reexamined every six months. One of several prominent "cohort studies" on HIV infection in the United States and around the world, the San Francisco Men's Health Study offered data of a kind that was simply not available at the time that closure had first been reached on the subject of HIV as the cause of AIDS.
In direct response to Duesberg's claims about Koch's postulates, Winkelstein organized his comments around what he described as a modern-day reformulation of those postulates, which consisted of five criteria. First, the "prevalence of disease should be significantly higher in those exposed to the factor than in unexposed controls." Winkelstein didn't have any data specifically on the prevalence of AIDS in the larger population, and his study (originally designed to examine progression to AIDS) had excluded from the outset any men already diagnosed with AIDS. But he did perform clinical and lab tests on his subjects upon entry, looking at a range of indicators considered to be predictors of AIDS, and the antibody-positive men had significantly higher prevalence rates for eighteen of the twenty-one indicators studied.
The second criterion was that incidence of disease (new cases) should be significantly higher in those exposed to the causal factor. This was precisely what Winkelstein had found. Thirty months into the study, of the 399 subjects who were antibody positive upon entry (all of them gay or bisexual), 13 percent had developed AIDS. Thirty-six subjects had seroconverted (become antibody positive) over the course of the thirty months; of these men, 8.3 percent had developed AIDS. And among 374 homosexual or bisexual men who remained seronegative throughout the thirty-month period, not a single person developed AIDS. Winkelstein estimated the probability that this association between antibody status and AIDS could have occurred by chance at less than one in a million.
According to the third criterion, a "spectrum of host responses" should follow exposure to the agent "along a logical biological gradient"; Winkelstein explained that this was demonstrated by the gradually declining T-cell counts in the antibody-positive group. Fourth, the disease must follow exposure to the causal agent: this criterion was confirmed by retrospective analysis of frozen sera that had been collected from gay men in San Francisco in 1978 for a hepatitis B vaccine study; analysis of the sera showed that gay men in San Francisco were
already infected before cases of the disease were known. And finally, elimination of the agent should decrease the incidence of cases: Winkelstein acknowledged that this criterion had yet to be satisfied, but he predicted that the decline in HIV transmission among gay men would eventually cause a corresponding decrease in the incidence of new AIDS cases.
During a lively question-and-answer period that followed the formal presentations, Anthony Liversidge, the interviewer who had elicited choice comments from Gallo, asked an important question about Winkelstein's data. Might not the same correlation between HIV infection and AIDS illness hold, asked Liversidge, if HIV were simply another opportunistic infection and not the actual cause of AIDS? Winkelstein acknowledged the point but argued that all the other evidence indicating a causal role for HIV made it highly unlikely that the correlation was "merely coincidental."
Opinion about the forum ranged widely in the gay and alternative press, from Ann Fettner's forthright denunciation of Duesberg as "homophobic" to Lauritsen's dismissal of the panel as a "kangaroo court." Interestingly, the AmFAR forum attracted a fair amount of attention in scientific publications but little in the mass media. (Possibly the mainstream reporters had lost interest once the apparent conspiracy of silence had ended, while by this point the larger scientific community was very much concerned about the potential ramifications of the controversy.) The position of reporters for both Science and Nature , the two most influential general science publications in the world, was that Duesberg had effectively been shown up. William Booth, writing his second article about Duesberg for Science , pointed to "vigorous head-shaking and audible groans" as Duesberg made his case. "If the … session accomplished anything," said Booth, "it was to confirm Duesberg as odd man out."
Writing in Nature , Rebecca Ward noted that the base of Duesberg's "credibility" all along had been "mainly among patient populations with the greatest interest in learning that HIV infection does not lead inevitably to a fatal disease," rather than among his scientific peers. At the forum, "Duesberg's quest for scientific credibility for his unorthodox theories … lost ground." Ward concluded with a prediction about the future course of the controversy, again distinguishing between Duesberg's popular credibility and his credibility in scientific circles: "Duesberg's theories will no doubt continue to receive attention from groups already mistrustful of the scientific establishment's
response to AIDS. But scientific acceptance for his ideas about AIDS, never very high, seems to be sinking." Little could Ward or Booth have guessed that, more than five years later, Duesberg would not only remain at the center of debate but would have garnered some backing from reputable scientists for his stance.
Part of Duesberg's capacity to attract credible support hinged on moving the debate more fully into respectable scientific circles. In April he published a brief restatement of his arguments in the British publication New Scientist (this was only weeks after the journal's editors, in an editorial called "And Yet It Kills," described Duesberg as "reveling in some peculiar form of intellectual self-indulgence"). But Duesberg's real coup was to force the AIDS establishment to debate him in the august pages of Science .
Here Duesberg was aided by Bialy, editor of Bio/Technology , who in March had written a letter to Dr. Daniel Koshland, the editor of Science and a colleague of Duesberg's at Berkeley: "I am very tired of hearing AIDS establishment scientists tell me they are 'too busy saving lives' to sit down and refute Peter's arguments [sic ] (although each one assures me they could 'do it in a minute if they had to'). … I urge you to use your offices to get Fauci or Gallo or Levy or Hazeltine [sic ], or Essex to prepare a rebuttal of Peter's arguments that is as carefully argued and referenced as his paper in Cancer Research." To simply dismiss Duesberg and hope he will eventually go away, concluded Bialy, "is a disservice and a disgrace to the very principles of scientific inquiry that you helped to teach me some twenty years ago."
Koshland solicited a short statement from Duesberg ("HIV Is Not the Cause of AIDS") and one coauthored by William Blattner (an NCI scientist), Gallo, and Temin ("HIV Causes AIDS") and ran the two statements, along with each party's response to the other, as a "Policy Forum" in the July 29, 1988, issue of Science . In their response to Duesberg, Blattner, Gallo, and Temin made what they saw as a crucial distinction between etiology (the cause of a disease) and pathogenesis (the processes by which the disease develops, including the mechanisms by which the etiologic agent causes the disease to be expressed). When he disputed whether HIV directly killed T cells and whether HIV was present in enough cells to cause immune system damage,
Duesberg was raising questions about pathogenesis. But while "there are many unanswered questions about the pathogenesis of AIDS, … they are not relevant to the conclusions that HIV causes AIDS." Recalling this turn in the debate some years later, Gallo would be adamant: "Never in the history of medicine have you had to solve pathogenesis before you could talk etiologically."
Why, then, were the authors so certain that HIV caused AIDS? In their contribution ("HIV Causes AIDS"), they made their case succinctly—though drawing less on virology, their area of expertise, than on epidemiological arguments: "The strongest evidence that HIV causes AIDS comes from prospective epidemiological studies that document the absolute requirement for HIV infection for the development of AIDS." Serology studies in the United States and around the world had demonstrated that wherever researchers found HIV, they would later find AIDS cases. The authors gave other examples. Over 95 percent of HIV-infected infants developed AIDS by the age of six, while their uninfected siblings never did. HIV, and not any other known infectious agent, was linked to transfusion-associated AIDS. And once HIV began to be screened out of the blood supply, the incidence of transfusion-associated AIDS began to decline, at least among new-borns who received transfusions. The authors provided one telling anecdote involving a baby that received a transfusion of HIV-tainted blood from a donor who later developed AIDS. The baby developed AIDS without any other risk factors, while the baby's mother and the baby's twin remained healthy. Blattner, Gallo, and Temin "conclude that there is overwhelming evidence that HIV causes AIDS."
Duesberg, however, was less than impressed by his colleagues' arguments. Epidemiology establishes correlations, Duesberg argued; it never proves causation. He went on to state than in order to establish a plausible causal model, researchers must make some sort of case that the putative cause is indeed capable of causing the disease in question. Pathogenesis, therefore, is never entirely dissociable from questions of etiology. In the past, when researchers have made causal claims in the absence of genetic or molecular evidence of activity, the results included, in Duesberg's words, "some of the most spectacular misdiagnoses in virology."
That said, Duesberg proceeded to address the epidemiological evidence presented by his interlocutors. First, he took exception to the claim that AIDS followed "in a predictable sequence" from HIV infection in all populations, noting once again that the incidence of AIDS,
expressed as a percentage of the group believed to be seropositive, seemed to vary widely between groups and between countries. Second, it was "presumptuous" to argue that HIV, rather than any other potential cause, was linked to AIDS in blood transfusion cases and in congenitally infected children. In the case of transfusions, how did we know that the recipients had no other risk factors during the years between infection and the development of AIDS? Besides, most of them were hemophiliacs, "persons with health risks … that are not representative of healthy individuals." As to the children, "96% had other health risks": their mothers were prostitutes or drug users, or the children had received blood products. So why assume that HIV was the culprit? These cases would be more convincing, Duesberg maintained, if the study authors had included a control group of matched antibody-negative persons and shown that they developed none of the AIDS indicator diseases or symptoms.
The Consequences of Controversy
What degree and what forms of credibility had Duesberg garnered in 1987 and 1988? On one hand, Duesberg's name and ideas, along with those of other dissenters, continued to surface in a variety of media and contexts. The gay magazine Christopher Street (owned, like the Native , by Chuck Ortleb) promoted alternative hypotheses of etiology in several more articles in 1988, and Duesberg entered the left-wing press with a positive treatment in the news-weekly In These Times . In a segment on AIDS treatments shown on the MacNeil/Lehrer News Hour , a San Francisco correspondent interviewed Duesberg, along with adversaries such as Winkelstein and Don Francis of the CDC. Jack Anderson wrote another column, focusing on Duesberg, Joseph Sonnabend, and Michael Callen, describing a "raging debate" over what caused AIDS, which was being enacted "behind the scenes of the AIDS crisis." Duesberg was also featured in a lengthy article in the popular scientific magazine Discover , which noted that he "doesn't look like a troublemaker" and that "even the Presidential Commission on AIDS recently listened to his testimony."
Moreover, there were signs throughout 1988 that Duesberg's views resonated with a small but not insignificant popular audience, particularly some gay men in cities throughout the United States. Volunteers at the San Francisco AIDS Foundation information hotline reported a
"small but growing number of calls about alternative theories regarding the cause of AIDS." And a number of activists were speaking out about the need to keep an open mind on the question of etiology. Michael Hirsch, founder of an advocacy group for HIV-positive people called Body Positive, was quoted in Christopher Street : "Body Positive feels very strongly that all possible theories and treatments should be explored. … Putting all our eggs in one basket is dangerous, as in the situation with HIV. AIDS has taught us that we have to assume responsibility for our own health. … We need to know about people like Duesberg and [Stephen] Caiazza [a proponent of the syphilis theory of AIDS causation], but the media is not going to tell us about them."
Finally, "AIDS establishment" scientists were increasingly forced, however reluctantly, to acknowledge the existence of controversy. "What is the evidence that HIV-I is the cause of AIDS? It is late in the history of HIV-I to bring this point up for review," complained Gallo in an overview of "HIV—The Cause of AIDS" published in 1988 in the Journal of Acquired Immune Deficiency Syndromes . "However, in the past year or so, those of us in the United States have seen the HIV-I cause of AIDS conclusion repetitiously, though not always thoughtfully, attacked by a few colleagues." The acceptance of their views, warned Gallo, "may lead to an irresponsible, carefree spread of the virus and progressive decline in the credibility of scientists, physicians, and health care workers."
But the most authoritative public representations of knowledge about AIDS showed little impact of the so-called "raging debate" beyond, in certain quarters, a perceptible hardening of positions. The 1988 update to the National Academy of Sciences' Confronting AIDS is instructive. In 1986, the report had questioned whether the term "AIDS" was still adequate to capture the full spectrum of conditions associated with HIV infection; by 1988, the authors were unequivocal: the actual disease being fought was the disease of HIV infection. "It is now clear that the 'AIDS epidemic' is really an epidemic of HIV infection, and when referring to the epidemic in general, we use the terms interchangeably." In 1986, the NAS authors had reviewed, without much passion, the evidence in support of the HIV hypothesis; but the 1988 update declared in boldface type: "The committee believes that the evidence that HIV causes AIDS is scientifically conclusive." The establishment line was presented without mention of dissent—yet the adamant tone of the presentation in comparison to that of two years
earlier suggested that Duesberg's opposition had mobilized scientific experts.
Another marker of authoritative knowledge was the report of the presidential commission, which appeared in 1988. Like the NAS, the commission tended toward a phenomenological merging of "HIV" and "AIDS," declaring in its "Executive Summary" that "the term 'AIDS' is 'obsolete.'" The commission maintained that "'HIV infection' more correctly defines the problem. The medical, public health, political, and community leadership must focus on the full course of HIV infection rather than concentrating on later stages of the disease." Such formulations, of course, left little room for doubt concerning the etiologic role of HIV. The phrase "HIV disease," the codification into language of a hegemonic belief, made it harder even to think the question of whether causality had been proven.
Consolidation and Refinement (1989–1991)
"Red Flags" at the Academy
Over the course of the next several years, Duesberg remained the most prominent of the "HIV heretics," and he engaged in a persistent struggle to keep his views before the eyes of a professional readership. By June 1988, before Science 's "Policy Forum" had even appeared in print, Duesberg had submitted another article, this time to the Proceedings of the National Academy of Sciences (PNAS ). The house organ of the same academy that had published Confronting AIDS, PNAS was unlikely to be receptive to Duesberg's views. Yet by virtue of having been inducted into the academy a few years earlier, Duesberg enjoyed a privilege unique in the world of scientific research: NAS members generally could publish in the Proceedings without submitting themselves to the rigors of formal, anonymous peer review. Instead, members were asked simply to show each submission to a knowledgeable colleague who could vouch for its worth and validity.
This special treatment was discretionary, however, and in practice PNAS suspended the policy in the case of manuscripts that raised the "red flag"—the managing editor's term for "things that have the possibility of ending up on the front page of the Washington Post ." The ambiguities of this policy had caused headaches for PNAS editors before, most notably in 1972, when the renowned scientist and academy member Linus Pauling was prevented from asserting in the journal's
pages that vitamin C could cure cancer. As Evelleen Richards has argued in a study of the Pauling controversy, PNAS 's gatekeeping practices reveal in particularly stark outline the "social character of the publication process" in science.
Duesberg's article was eventually published by PNAS in February 1989, with a second one to follow two years later —yet the behind-the-scenes politicking attracted more attention than the articles themselves. Writing another news report for Science , William Booth described the "60 pages of correspondence" generated by "nearly 8 months of protracted, often testy, occasionally humorous negotiations" between Duesberg and Igor Dawid, the chairman of the editorial board. Dawid's predecessor, Maxine Singer, had rejected Duesberg's 1988 submission outright on the grounds that it repeated the arguments in Cancer Research and therefore lacked originality. Maintaining that the article had one hundred new references, Duesberg pressed his case, and Dawid, having taken over from Singer, passed the paper along for peer review by three anonymous reviewers, all of whom raised objections to the manuscript. "For the next 6 weeks," said Booth, "by express mail and by fax machine, Duesberg and Dawid duked it out," with Duesberg agreeing to a number of changes and clarifications. Booth suggested that Dawid eventually surrendered to the inevitable; he quoted from Dawid's correspondence: "At this state of protracted discussion I shall not insist here—if you wish to make these unsupported, vague, and prejudicial statements in print, so be it. But I cannot see how this could be convincing to any scientifically trained reader." In truth, what Dawid may have failed to see was that Duesberg could later use the very fact of having been published in the Proceedings as capital to advance his position.
Anthony Liversidge, writing a longer piece for The Scientist , raised the more nettlesome questions about "just what constitutes fair play in the science publishing arena." On one hand, it seemed problematic to have a special publication policy for academy members that was applied only selectively. On the other hand, what was the point of insisting that the paper be peer reviewed if in the end the journal was going to publish it anyway, despite the fact that all three reviews were unfavorable? Liversidge quoted Walter Gilbert, a professor of molecular biology at Harvard and winner of the 1980 Nobel Prize for his work on DNA sequencing methods, who criticized the PNAS editors for giving Duesberg "too much of a rough going." But opponents of Duesberg, such as Gallo—who said he hadn't read the paper because "I have
to work for a living"—simply chalked up the incident to the peculiarities of PNAS 's policies: "The Proceedings is a great journal, but you can't stop a member from publishing unless it is totally off the wall."
Arenas of Controversy
Besides the articles in the Proceedings , there were three other important arenas in which the controversy was played out in the period from 1989 to 1991. First, debate about the etiology of AIDS invaded the International Conference on AIDS in San Francisco in 1990: at a specially convened session, Luc Montagnier placed himself in the camp of Shyh-Ching Lo by announcing that he had found a mycoplasma in a significant percentage of AIDS patients (thirty-seven out of ninety-seven). Montagnier proposed that the mycoplasma might be a necessary cofactor that acts in conjunction with HIV to cause AIDS. The antibiotic tetracycline, by killing the mycoplasma, might therefore be of benefit to AIDS patients. In particular, Montagnier thought that a cofactor such as mycoplasma could explain how HIV caused the destruction of the immune system, given that the virus was not found in many cells and given that the virus did not appear to kill cells directly. U.S. scientists were dismissive of Montagnier's new hypothesis. "Dr. Montagnier is out on a limb," said James Curran, director of the AIDS program at the CDC. Some scientists expressed the view that Montagnier was squandering his credibility; in the words of the New York Times , they "[wondered] aloud why Dr. Montagnier would risk his professional standing by backing such a theory without more evidence."
Later, HIV dissenters would reap support by pointing to the way the "orthodox" had silenced one of their own when he dared to step out of line. Duesberg would indirectly benefit from Montagnier's intervention, effectively riding on the coattails of the French scientist in the mainstream media. At the 1990 conference, however, this San Francisco Bay Area resident was far from the action. At a hotel two blocks away from the official conference, Duesberg addressed a symposium on alternative treatments for AIDS. A dismissive report by a Reuters correspondent described the mix of alternative treatments proposed by the panelists as "a witch's cauldron of boiling blood, mushrooms and mistletoe," and associated Duesberg with this imagery by noting that "his contentious theory … has brought charges of 'quackery' against him."
Duesberg fared better in a different arena, a British television documentary called "The AIDS Catch," produced by Joan Shenton and Meditel Productions, who had already featured Duesberg once, in 1988. Shown on British television in June, just before the International Conference, the program ignited a firestorm in Britain by presenting the world of AIDS as seen through the eyes of the HIV dissenters. As the narrator declared: "Everything we currently accept about AIDS can be turned on its head." The narrator presented a range of questionable statistics, noting that in any one year in the United States, only a tiny fraction (1.5 percent) of HIV positives develop AIDS, but not indicating how many HIV positives develop AIDS over longer periods of time. In an argument against AZT, the show also claimed that "so far no one has lived longer than three years" on the drug, without explaining that AZT had not been in general use for much longer than that and that only the sickest patients had initially been prescribed it.
"The AIDS Catch" assembled in one place nearly all of the key dissenters. Duesberg was featured prominently on the show, along with Sonnabend and Callen. Lauritsen presented his observations on gay male culture, telling the interviewer: "They might take six different drugs in the course of an evening." British writer Jad Adams, whose pro-Duesberg book, AIDS: The HIV Myth , was published the previous year, proposed psychological reasons for why "people want to believe in HIV." Gordon Stewart, an epidemiologist from Glasgow who supported the immune overload hypothesis, discussed poppers, which he described as "very toxic indeed." The program also featured Walter Gilbert, the Nobel Prize-winning Harvard molecular biologist who had criticized PNAS in the interview with Liversidge. Gilbert was persuaded by the substance of many of Duesberg's arguments, but he made his most forceful point with reference to what he called "democratic theory," arguing that scientific progress comes about through the clash of opposing ideas: "The great lesson of history is that knowledge develops through the conflict of viewpoints, that if you have simply a consensus view, it generally stultifies, it fails to see the problems of that consensus; and it depends on the existence of critics to break up that iceberg and to permit knowledge to develop. This is, in fact, one of the underpinnings of democratic theory; it's one of the basic reasons that we believe in notions of free speech; and it's one of the great forces in terms of intellectual development."
The Heritage Foundation
and the "Risk-Aids Hypothesis"
The third crucial arena for dissenting views during this time period was a lengthy (8,900-word) cover story by Duesberg and Bryan J. Ellison published in the summer 1990 issue of Policy Review, a publication of the Heritage Foundation, the well-known, right-wing think tank. The essay was actually written by Ellison, a politically conservative graduate student in Duesberg's department and self-appointed popularizer of Duesberg's views. "Scientists weren't going to listen to him. They couldn't afford to," Ellison explained. "So I realized he had to take his case to the general public." The article became, in the editor's words, "one of the three or four most-talked-about articles in the history of the magazine, … [eliciting] more letters to the editor than any in Policy Review 's history." The article also incorporated the first formal presentation by Duesberg of an alternative explanation for the etiology of AIDS, which Duesberg and Ellison dubbed the "risk-AIDS hypothesis."
The biographical note explained that Duesberg had published critiques of the accepted "virus-AIDS hypothesis" in a number of scientific journals, such as Cancer Research and the Proceedings of the National Academy of Sciences . In this way, Duesberg's accumulated scientific credibility was now converted into credibility in a different, more public forum. However, a chief strategy of the Policy Review article was to present the critique not as Duesberg's personal crusade, but as the clamor of a growing chorus, within which Duesberg was just one voice. The article therefore attributed dissenting views whenever possible to people like Walter Gilbert and Harvey Bialy. More generally, it described "an increasing number of medical scientists and physicians [who] have been questioning whether HIV actually does cause AIDS"; the article linked together those who said HIV could not play a role, those who said HIV had not conclusively been proven to play a role, and those who argued for cofactors. The reader might never have heard of this expanding group, the authors explained, because "most of these doubters prefer not to be quoted, out of fear of losing research funding or of disapproval by peers." Skepticism therefore remained a minority position "due largely to inadequate attention provided by media sources."
In the article, Duesberg and Ellison reiterated their standard arguments but also presented in expanded form a criticism that Duesberg
had not previously discussed in print in great detail: they argued that the notion that HIV caused AIDS was based fundamentally on a tautology. According to the CDC's 1987 update of its surveillance definition, AIDS was (usually) diagnosed by a positive HIV antibody test, in the presence of one or more diseases from a list: "The disease-list includes not only Kaposi's sarcoma and P. carinii pneumonia, but also tuberculosis, cytomegalovirus, herpes, diarrhea, candidiasis, lymphoma, dementia, and many other diseases. If any of these very different diseases is found alone, it is likely to be diagnosed under its classical name. If the same condition is found alongside antibodies against HIV, it is called AIDS. The correlation between AIDS and HIV is thus an artifact of the definition itself." Perfectly ordinary illnesses got stuck with the label "AIDS" if the ill person happened to be HIV positive; then researchers would turn around and say that, since everyone with AIDS was HIV positive, HIV must be the cause. This was an interesting argument, one which threw into question not only the logic of the causal claim but also the very status of "AIDS" as a legitimate disease category. It was an argument that Duesberg would often repeat in subsequent years; but it was somewhat disingenuous as posed.
Although the CDC's 1987 definition listed a number of diseases that, in an HIV-infected person, would result in an AIDS diagnosis, many of them—like Pneumocystis carinii pneumonia, toxoplasmosis, and cryptosporidiosis, diseases typical of AIDS patients—were relatively rare in general. Others, like CMV, herpes, and candidiasis, were indeed common, but in these cases the CDC's specifications went further, requiring that the conditions be present in parts of the body where these infections normally did not take root. Similarly, tuberculosis was on the list—but only if it involved at least one site other than the lungs. Diarrhea, of course, was not on the list; Duesberg and Ellison were referring casually to what the CDC called the "HIV wasting syndrome," defined as "profound involuntary weight loss > 10% of baseline body weight plus either chronic diarrhea (at least two loose stools per day for > 30 days) or chronic weakness and documented fever (for > 30 days, intermittent or constant) in the absence of a concurrent illness or condition other than HIV infection that could explain the findings. …" The diagnostic definition of AIDS-related dementia was similarly restrictive. Overall, clinical markers of AIDS were rare diseases and conditions generally not seen in people who were not HIV positive. By failing to explain these details of the CDC's diagnostic algorithm and by suggesting that ordinary diarrhea and tuberculosis
were being taken as markers of AIDS, Duesberg and Ellison were misleading their lay audience.
But at the same time, Duesberg and Ellison presented arguments to counter the assumption that the rare AIDS diseases, like Kaposi's sarcoma and PCP, were in fact so rare. They maintained that "not only have all 25 of these AIDS conditions existed for decades at a low level in the population, but HIV-free instances of the same diseases are still being diagnosed." They also described a recent letter to Lancet by Robert Root-Bernstein, an associate professor of physiology at Michigan State University and recipient of a MacArthur fellowship—one of the so-called "genius grants" provided, no-strings-attached, to individuals in a variety of fields who have been deemed unusually promising. Root-Bernstein's review of the medical literature had led him to conclude that perhaps 15 to 20 percent of all Kaposi's sarcoma cases before 1979 fit the pattern generally believed to have arisen only with the AIDS epidemic: young victims with a short survival time. Citing Sonnabend, Root-Bernstein had written: "Several hypotheses must be entertained—that AIDS is not new; that HIV is only one of several possible causes of AIDS; or that HIV is itself a new, opportunistic infection that takes advantage of previously immunosuppressed individuals."
The existence of "AIDS" diseases in people who are not antibody positive, in Duesberg and Ellison's view, was evidence for their alternative hypothesis, the risk-AIDS hypothesis. They proposed "that the AIDS diseases are entirely separate conditions caused by a variety of factors, most of which have in common only that they involve risk behavior." But like Sonnabend and others who had trod this path before them, the authors recognized that "a risk hypothesis must explain the recent increases in the various AIDS diseases, and why these have all been concentrated in particular risk groups." So Duesberg and Ellison put forward a potpourri of potential causes of the AIDS marker illnesses, linking Kaposi's sarcoma with popper use by gay men; AIDS dementia with psychoactive drugs and syphilis; and the wasting syndrome, "found most heavily in African AIDS patients," with "the extremes of malnutrition and the lack of sanitation on most of that continent," compounded in recent years by "wars and totalitarian regimes."
Many of these arguments were widely familiar from debates early in the epidemic: the claims about African health conditions, for example, mirror Sonnabend's speculations about Haitians in 1983. And indeed, to explain the systemic failure of immune response that is
characteristic of AIDS, Duesberg and Ellison's article explicitly endorsed the immune overload hypothesis, incorporating it within their risk-AIDS hypothesis: "Joseph Sonnabend, a New York physician who founded the journal AIDS Research in 1983, has pointed out that repeated, constant infections may eventually overload the immune system, causing its failure; still worse are simultaneous infections by two or more diseases." Duesberg and Ellison also pointed to heavy drug use as a major cause of immunosuppression. They claimed that abuse of alcohol, heroin, cocaine, marijuana, Valium, and amphetamines "can all be found as part of the life histories of many AIDS patients"; "when combined with regular and prolonged malnutrition, as is done with many active homosexuals and with heroin addicts, this can lead to complete immune collapse." To round out the picture, the authors noted the long-term immunosuppressive effects of antibiotics and claim that "active homosexuals … often [take] large amounts of tetracycline and other antibiotics each evening before entering the bath houses."
Duesberg and Ellison didn't provide any sources for their ethnographic data, and in interviews both of them acknowledged having little direct knowledge of gay life despite its vibrant expression in San Francisco, only miles from the Berkeley campus. In part the authors were drawing on early medical claims about "how the gay lifestyle" was related to the epidemic of immune suppression, which in turn borrowed from earlier and contemporary medical literature on gay men who attended clinics for treatment of sexually transmitted diseases (see chapter 1). Communication with John Lauritsen may also have played its part in shaping their biased understandings of gay male behavior. In a letter to Duesberg written just a few months earlier, Lauritsen had characterized the Mineshaft, the Saint, and St. Mark's Baths—the most prominent New York City venues for uninhibited gay male sex in the years before the epidemic—as "hell-holes which were the arenas for truly psychopathic drug abuse as obligatory tribal ritual."
Gay men and injection drug users had always been the focus of immune overload theories. But no one promoting such a perspective in 1990 could avoid discussion of the other "risk groups," and Duesberg and Ellison understood this. They explained (again echoing Sonnabend's claims from seven years earlier) that blood transfusion recipients were at risk of developing immunodeficiency because of pathogens present in transfused blood. Moreover, people receiving blood
transfusions typically did so because they were already quite ill or had undergone surgery, and both the trauma of the surgical procedure and the anesthesia could have immunosuppressive effects. In fact, Duesberg and Ellison claimed, "with or without HIV infection, half of all [transfusion] recipients do not survive their first year after transfusion." Similarly they noted that "hemophilia has always been a fatal condition," and that the blood products received by its sufferers were immunosuppressive. Finally, cases of AIDS in infants could be traced to "combinations of most of the above risk factors"; 95 percent of these babies were born to mothers who either used drugs or were sex partners of drug users, or had received transfusions, or had hemophilia. According to Duesberg and Ellison: "The risk behavior of many of their mothers has reached these victims, but their conditions are renamed AIDS when in the presence of antibodies against HIV."
In the conclusion to the article, Duesberg and Ellison turned to the policy implications of their argument. "The most urgent of these," they said, concerned the widespread administration of AZT. This powerful drug worked by inhibiting the replication of the virus, but "by doing this the drug also kills all actively growing cells in the patient," including immune system cells. If the virus was harmless, as the authors maintained, then "inhibiting HIV would accomplish nothing, while AZT actually produces the very immune suppression it is supposed to prevent." AZT, by this view, was just another harmful drug—like heroin, cocaine, and poppers—that contributed to immune overload. Second, the risk-AIDS hypothesis called into question the existing AIDS education strategies. Condoms and sterile needles were fine if the goal was to prevent hepatitis and other infectious diseases. But the hazard of these programs, Duesberg and Ellison maintained, was that they lulled the practitioners of risk behaviors into a false sense of security. By failing to "[emphasize] the danger of the risk behavior itself—particularly drug-taking—[these programs] may inadvertently encourage spread of the disease."
The HIV hypothesis "has not yet saved a single life, despite federal spending of $3 billion per year," Duesberg and Ellison reminded their readers in closing. Instead of sinking more money down the same hole, the government should begin funding "studies on the causes of the separate AIDS-diseases and their appropriate therapies." The rest of the $3 billion "might then be saved and returned to the taxpayers," wrote the authors in a suggestion that presumably did not clash with the conservative agenda of Policy Review .
The next issue of the magazine was devoted to letters in response to Duesberg and Ellison—the total length of the letter section was over 13,000 words, one and a half times the length of the original article. Both the establishment and the dissenters were well represented. Howard Temin stressed the "tragic" pediatric evidence: in one study, fifteen of sixteen HIV-infected children of infected mothers had AIDS or pre-AIDS symptoms, while none of thirty-nine uninfected children of infected mothers showed signs of illness. Wrote Temin: "Duesberg and Ellison state that 'the risk behavior of many of their mothers has reached these victims.' It is clear that what reached the children was HIV." Warren Winkelstein, the Berkeley epidemiologist, wrote in with the most recent results from the ongoing San Francisco Men's Health Study. Out of 386 homosexual men who had been HIV positive when entering the study six years before, 140 (36 percent) had developed AIDS, and the majority of them had died. Forty homosexual men had become infected since entering the study, and 2 (5 percent) had developed AIDS. But of 370 homosexual men who had remained uninfected, none developed AIDS.
An interesting letter came from Michael Fumento, who had written a popular book called The Myth of Heterosexual AIDS . Each of them a controversial figure, Duesberg and Fumento shared the belief that AIDS was a "risk group disease" and not a threat to the general population. But they were on opposite sides when it came to the etiological debate. Noting that his "initial reaction to anyone challenging the AIDS industry in any way is favorable," Fumento continued: "but in the case of Peter Duesberg and his co-author Bryan Ellison, I really must demur." After raising objections to Duesberg and Ellison's arguments, Fumento threw down the gauntlet: "What I would suggest, in perfect seriousness, is that before the authors write another article suggesting that it is perfectly okay for HIV-infected persons to have unprotected sex with uninfected persons or vice-versa, that they, in a public forum, inject themselves with HIV. Apparently Duesberg has hinted he may do it; I think he should go beyond that. Readers have a right to know just how much faith the authors have in their own theory."
Duesberg and Ellison were given the last word, and they had plenty to say. They began by expressing their pleasure that "the debate that should have occurred … years ago" was finally taking place. They then launched into a critique of the cohort studies that Winkelstein
and other letter writers had cited as definitive. The existing studies proved nothing, in Duesberg and Ellison's view, because they failed to demonstrate that illness was the consequence of HIV, not risk behavior. A controlled study actually designed to distinguish between the two causal hypotheses would be set up quite differently. It would compare two large groups of people, HIV positives and HIV negatives. But the two groups would be carefully matched for "every health risk that might possibly be involved in the various AIDS diseases."
Duesberg and Ellison also responded to various arguments that letter writers had raised—about babies with AIDS, about wives of hemophiliacs, about needle-stick injuries. Only "media sensationalism," they argued, could convince people that wives of hemophiliacs were at great risk of AIDS if they had no other risk factors. Those cases that had occurred were quite explainable: "Since AIDS is merely, by definition, a list of old diseases that are renamed when in the presence of antibodies against HIV, one should not be surprised to find an occasional such wife who happens to contract HIV and, coincidentally, one of the many diseases on the AIDS list." A controlled study, they believed, would show that HIV-positive wives developed AIDS indicator diseases at the same rate as HIV-negative wives.
The real problem, in Duesberg and Ellison's view, was that the established AIDS researchers abandoned scientific principles when it suited their interests. Instead of controlled studies, these researchers invoked anecdotal evidence. When Koch's postulates failed them, they "casually try to abandon those timetested, commonsensical" rules of scientific method. And "when all else fails," they started "changing the rules," "rather than bringing the hypothesis into question," as real scientists were supposed to do. To explain why so few antibody-positive people had AIDS, "a latent period first had to be invented, then extended to its present, and still growing, total of 10 to 11 years." Duesberg and Ellison concluded by declaring themselves "quite willing to carry out the Fumento test." But their degree of interest in doing so depended on the attention it could attract to their cause: "If he will arrange for sufficient national publicity, if he would be convinced by our action, and if he will thereafter help us bring exposure to our viewpoint, we will indeed be quite happy to have ourselves publicly injected with HIV. Perhaps Fumento will also be willing to check on our health status in the year 2000, or after whatever additional time is eventually added to the virus' latent period."
"The Impact of the Truck"
The International AIDS Conferences, the documentary "The AIDS Catch," and the Policy Review article and ensuing debate were three arenas in which the causation controversy bubbled into clear public view in 1989, 1990, and 1991. Elsewhere, the controversy was not invisible, but it simmered more quietly. In scientific communities and gay communities, in the mainstream press and the alternative press, various players pushed their claims, seeking to establish their credibility or undercut that of others. In the process, dissenters who had been predicted to fade into oblivion instead demonstrated their staying power. This quiet jockeying for position would set the stage for a fierce resurgence of the causation controversy in 1992.
Formal scientific debate continued throughout this period. One exchange that was followed closely by insiders took place in the Journal of Acquired Immune Deficiency Syndromes between Duesberg and Alfred Evans of the Department of Epidemiology and Public Health of the Yale University School of Medicine. Evans was an authority on Koch's postulates and had been writing about them since the 1970s; he emphasized that "the postulates of causation have changed and will continue to change with the new technology and new concepts of pathogenesis." Revealing his historical bent, Evans also noted that Duesberg's offer to be injected with HIV was reminiscent of a similar act by German researcher Max von Pettenkofer. In 1892 at the age of seventy-four, von Pettenkofer drank a milliliter of "a fresh culture of cholera vibrio derived from a fatal case" to attempt to prove his point that cofactors were required to cause the disease. Von Pettenkofer was lucky: he didn't develop serious cholera, although he did have gas and diarrhea for a week afterwards. Evans urged Duesberg not to follow in von Pettenkofer's footsteps.
Duesberg also published articles and letters in Science, Nature, The Scientist , the New England Journal of Medicine , and the Pasteur Institute's Research in Immunology , among other places. In these publications Duesberg tended to restate his earlier views while responding to critics. Increasingly, he invoked other dissenters as allies in his writings, citing work by scientist and nonscientist alike—Jad Adams, Celia Farber, John Lauritsen, Harry Rubin, Joseph Sonnabend, Katie Leishman, Anthony Liversidge, and Gordon Stewart. Robert Root-Bernstein, the young physiologist whose letter to Lancet had attracted Duesberg's notice, also kept busy. He expanded on his position in a
1990 article in a journal called Perspectives in Biology and Medicine . Although careful to maintain an official position of agnosticism, Root-Bernstein stressed the prevalence of risk factors among people with AIDS—chronic or repeated infectious diseases, drug use, anesthetics, antibiotics, semen exposure, blood exposure, and malnutrition.
For the average layperson not inclined to peruse the pages of the medical and scientific journals, the easiest place to learn about the HIV dissidents during this time period was, ironically enough, the pages of Robert Gallo's Virus Hunting , a book for the general reader published in 1991. Though in the past Gallo had declared himself "too busy" even to bother reading Duesberg's articles, this book included an entire chapter entitled "About Causes of Disease (and, in Particular, Why HIV Is the Cause of AIDS)"—a chapter that, amid discussion of Montagnier's mycoplasmas and Root-Bernstein's risk arguments, devoted a full ten pages to refuting Peter Duesberg.
"When are we ready to say that we know the cause of a disease?" asked Gallo, taking aim at the crux of the controversy. "To a greater extent than we might want to believe, there are few hard-and-fast rules [and] certainly no cookbook recipe to follow," he added, noting that Robert Koch "has been taken too literally and too seriously for too long." But most diseases did have a sine qua non , though other factors might contribute to the severity, speed of onset, or likelihood of development. Gallo offered the analogy of head injury in the case of a truck that crashes into a group of bicyclists, some of whom are wearing helmets, some of whom hit concrete, and some of whom are clad in red shirts: "We could argue that the cause of the head injury was concrete, the red shirts, the absence of a helmet, or the truck—but we don't. The impact of the truck is the sine qua non , the cause. The others are influential positive or negative factors or correlations with no influence at all, as in the case of the red shirts." "Of course there are diseases where there is true multifactorial [causation]," Gallo later commented, reflecting on the etiology of some types of cancer. But "HIV causes AIDS, nothing else: you take it away, [AIDS] goes away."
Gallo's book did not dispute the possibility of contributing causes—indeed, over the past few years, he had been proposing that a virus called HHV-6 (human herpes virus, number six) might speed up the process by which HIV destroyed T cells. But HIV could also do its work without HHV-6, while HHV-6 alone did not cause AIDS. HIV, in other words, was both a necessary and sufficient cause. Montagnier,
by contrast, was now proposing that a mycoplasma might be a second necessary cause along with HIV—a claim that Gallo found "astonishing." Montagnier's cofactor theory provided "added longevity to confused and confusing … arguments that HIV is not the primary cause of AIDS," Gallo complained. What particularly irked him was that Montagnier had thereby "lent some support to Duesberg (who, interestingly enough, dismissed Montagnier's idea)."
Gallo could hardly deny that Montagnier had impressive credentials for commenting on questions of medical science. But he was quick to observe that "the vast majority of people who have raised, re-raised, and re-re-raised objections to the conclusion of an HIV cause of AIDS"—here Gallo names Jad Adams, Katie Leishman, Anthony Liversidge, and Chuck Ortleb—"seem to have little or even no experience in science or medicine." What of Duesberg? Gallo acknowledged his colleague's indisputable scientific accomplishments, but stressed that they might not have prepared him to comment credibly on AIDS: "He made very significant contributions to our understanding of the molecular biology of animal (especially chicken) retroviruses many years ago and is a member of the National Academy of Sciences. On the other hand, he is not an epidemiologist, a physician, or a public health official. More important, to my knowledge Duesberg has never worked on any naturally occurring disease of animals or on any disease of humans, including AIDS. Nor, I believe, has he ever worked with HIV."
During the 1989–1991 period, Duesberg also continued to receive publicity in the mass media, including a long and generally sympathetic feature article by Garry Abrams in the Los Angeles Times that asked whether the scientist was "Hero or Heretic." Abrams noted that Duesberg was shocked to learn in fall 1990 that the NIH had declined to renew his five hundred thousand-dollar-a-year Outstanding Investigator Grant. While renewal of such grants is far from automatic, the review committee had written that Duesberg had become "less productive, perhaps reflecting a dilution of his efforts with non-scientific issues." This was a serious blow to Duesberg, and Abrams implied that it was direct punishment for heresy, with the phrase "non-scientific issues" serving as a euphemism for Duesberg's campaign against the orthodox position on AIDS.
One symptom of the thickening of debate was that the media began covering the media coverage. USA Today ran an article on Spin magazine, "the only general interest publication pushing [Duesberg's] theory."
Charles Trueheart reported on the Policy Review debate for the Washington Post , suggesting that the authors' emphasis on the role of personal behavior in the cause of AIDS "may explain why their article appears in this conservative journal."Lies of Our Times , an alternative magazine dedicated to policing the writings of the New York Times , complained that the newspaper had never mentioned Duesberg since Philip Boffey's original article in 1988, and it claimed that "the silence of the Times kept Duesberg out of the major media for three years."
Duesberg also was promoted in places like the New York Native by authors like Lauritsen. Elsewhere in the gay press, the causation controversy was a marginal issue but one that provoked periodic heated exchanges. Writing in the Bay Area Reporter , a San Francisco gay newspaper, columnist and AIDS activist Michael Botkin described the "peculiar revival of interest" in Duesberg's theories. Duesberg "continues to be shunned by virtually all serious AIDS activists," wrote Botkin, "but has sparked some interest from heterosexual, HIV-negative, radical-posing journalists." But while some commentators worried about the consequences of knee-jerk anti-expertism, others expressed the opposite concern—that gays were inexplicably naïve and were following the medical establishment like placid sheep. In a discussion of Duesberg's arguments and Montagnier's "startling admission," Ralph Garrett wrote to the San Diego Gay Times: "In the face of such a scandal, among the questions we in the gay community should be asking ourselves is how could we have credulously surrendered our lives and deferred our better judgement to an authority which has proved to be just as corruptible as any other? … What madness could have come over us?"
From Outside to Inside and Back Again
Conventional views of science presume a top-down model of knowledge dissemination. True ideas originate within a select community of educated specialists; from there, they percolate "downward"; eventually, in watered-down or distorted form, they penetrate the consciousness of the masses. But as Stephen Hilgartner has argued, this model fails to capture the ways in which "popularized knowledge feeds back into the research process." Duesberg's views on AIDS are an interesting example. Early in the epidemic, ideas about
"immune overload" diffused from researchers to doctors and patients and were taken up by lay theorists such as Callen and Lauritsen. Many of these same ideas then reemerged in the scientific articles of Duesberg, who cited the lay publications in his footnotes and thanked their authors in his acknowledgments. As Hilgartner noted, "when one looks carefully for the precise location of the boundary between genuine scientific knowledge and popularized representations, one runs into trouble. …"
There is still another sense in which the pursuit of scientific credibility by Duesberg reveals the considerable permeability of boundaries between the "inside" and the "outside" of science in the case of AIDS. On one hand, Duesberg's success in promoting his views depended heavily on his status as an "insider." As of 1986, dissenting voices on the causation of AIDS were marginalized, and they might have remained so had someone with the scientific credibility of Peter Duesberg not entered the debate. On the other hand, Duesberg's capacity to sustain his critique then depended heavily on support from "outside." His article in Cancer Research might have gathered dust on library shelves, if not for the active promotion of his views by a group of lay supporters who succeeded in pushing the controversy into the mass media. This publicity led to Duesberg's presentation of his arguments in official forums, such as the AmFAR conference, Science , and PNAS . By extending his credibility from one arena to another—using his scientific credentials to buy him popular support, then using the popular support to push for recognition by his colleagues—Duesberg gained staying power. The next chapter describes how Duesberg sought to continue his battle and how the "AIDS establishment" responded.
The Debate That Wouldn't Die
The Controversy Reignites (1991–1992)
From Isolation to Organization
In mid-1991, the struggle by Duesberg and other HIV dissenters to create credibility for their claims in both popular and professional arenas was given a significant boost by the founding of an organization. The impetus came from a molecular biologist named Charles Thomas Jr., a former Harvard professor and current director of a small biotechnology research institute in San Diego. Thomas later commented that he believed "it was a matter of civic duty" to get involved, saying, "I've worked on viruses and I can read and understand this literature. … I felt real fabrications were taking place."
The group took form in a flurry of faxes between Thomas, Duesberg, Robert Root-Bernstein, Berkeley law professor Philip Johnson, and an actuary from Kansas City named Robert Maver. Thomas originally dubbed the organization "Friends of HIV," and, in a "Dear Colleague" form letter mailed to potential supporters, he asked them how they liked the title. In the end, sobriety prevailed over facetiousness and the organization became the "Group for the Scientific Reappraisal of the HIV/AIDS Hypothesis." The group submitted a statement to both Science and Nature in June 1991 and asked that it be published as a letter to the editor. The full statement read: "It is widely believed by the general public that a retrovirus called HIV causes the group of diseases called AIDS. Many biomedical scientists now question this
hypothesis. We propose that a thorough reappraisal of the existing evidence for and against this hypothesis be conducted by a suitable independent group. We further propose that critical epidemiological studies be devised and undertaken."
The letter was notably restrained in tone and in content. By calling simply for reappraisal and by not advocating an alternative hypothesis or making any of the more controversial claims that had been advanced earlier by Duesberg and other dissenters, the letter was well suited to attract support. It went to Nature and Science with twenty-eight signatures, and by the following year Thomas had gathered a total of fifty-three. The signatories were mostly from the United States, but there were a few from Switzerland, Italy, Britain, Germany, and Australia. The list included familiar names, like Harvey Bialy, Gordon Stewart, and John Lauritsen. But others were new to the public controversy, and many of them came with respectable credentials. Of the fifty-three who had signed by June 1992, twelve had M.D.'s and twenty-five had Ph.D.'s. Twenty of the fifty-three gave academic affiliations with departments like physiology, biochemistry, medicine, pharmacology, toxicology, and physics.
Yet remarkably enough, the letter never saw publication, having been rejected not only by Nature and Science , but by Lancet and the New England Journal of Medicine as well. While this gatekeeping may have kept a minority view out of the prestigious scientific and medical publications, it also guaranteed favorable publicity for the group in the mainstream media. One journalist with the San Diego County edition of the Los Angeles Times interviewed Thomas and wrote a story focusing on the suppression of dissent and the plague of "political correctness" in biomedicine. The Chronicle of Higher Education also profiled the group in December 1991, in an article that described Duesberg's fight to recover his Outstanding Investigator Grant and noted that Duesberg's representative in Congress, Ron Dellums, had looked into the NIH's handling of the grant application.
Meanwhile, backing for Duesberg arrived from an unlikely quarter. "Professor Peter Duesberg … is probably sleeping more easily at night," suggested John Maddox, the editor of Nature , in a September 1991 piece in the "News and Views" section called "AIDS Research Turned Upside Down." Maddox summarized two recent and perplexing studies that suggested the presence of autoimmune mechanisms in the development of AIDS. "None of this would imply that HIV is irrelevant to AIDS," Maddox concluded, "but that an immune response to foreign cells, most probably lymphocytes, is also necessary.
Duesberg will be saying, 'I told you so.'" In the past, "Duesberg has been pilloried for his heterodox views … and faced with the threat that his research funds would be snatched away," wrote Maddox. "Now there [is] some evidence to support his long fight against the establishment (among which, sadly, he counts this journal)."
"Pilloried Professor May Be Right about Aids," proclaimed London's Daily Telegraph . "New Study Vindicates Duesberg, Calls AIDS an Autoimmune Disease" read an article in the Bay Area Reporter . Others were more cautious in their conclusions. A reporter for Science , in an article called "Duesberg Vindicated? Not Yet," cited "numerous … researchers [who] failed to see any connection between [the two studies] and the stand taken by Duesberg." One of the researchers whose article had provoked the fuss told Science: "We have nothing in common with [Duesberg's] idea that HIV has nothing to do with AIDS." No fan of the autoimmune hypothesis himself, Duesberg agreed, saying "Those studies have nothing to do with [my position]."
Joseph Palca, the reporter for Science , focused on Maddox's motives for endorsing Duesberg, given that Duesberg occupied such an extreme position in the debate. Maddox explained to Palca: "I'm not for a minute saying Duesberg is right in all points. But I feel sorry that Nature has not done more to give his view prominence. It would have hastened the process by which the scientific community is coming around to the view that the pathogenesis of AIDS is more complicated than the baby-talk stories we were all given a few years ago." This was the real issue, Joseph Sonnabend commented in a column in the gay and lesbian magazine NYQ —the "vast gulf between the simplistic view of the pathogenesis of AIDS that has been presented by those who lead the AIDS research establishment … and the painful reality that we have almost no understanding of the pathogenesis of this disease." The "baby-talk story"—that HIV causes AIDS in all infected people by directly killing T cells and that the only cofactor is the passage of time—"was not arrived at as the result of years of intense and painstaking research," Sonnabend complained, "but was almost instantly discovered in 1984, and presented not as speculation but as established fact."
The "Drug-Aids Hypothesis"
As the implications of Maddox's intervention were sorted out in various arenas, Duesberg scored another partial victory:
the publication in a professional journal of a formal statement of his own hypothesis as to the causes of AIDS. The article was published in Biomedicine & Pharmacotherapy after a yearlong, ultimately unsuccessful, campaign by Duesberg to publish once again in the far more prestigious Proceedings of the National Academy of Sciences . The Proceedings had published Duesberg's views on AIDS twice before but each time had sent the submissions out for peer review, breaking with its ordinarily relaxed procedures for academy members. Both times the reviews had been critical; both times editor Igor Dawid ultimately had relented. This time Dawid put his foot down, writing Duesberg in February 1991 that the article had been rejected. One referee had called the paper a "flight of ideas" and "grossly incomplete," while the second referee favored publication. The third referee acknowledged, "I am no expert in the fields concerned" and made a political argument: "In all likelihood the publication of this article in PNAS would be harmful to the reputation of the journal, and has a potential for being harmful to the HIV infected segment of the population."
What was all the fuss about? In "The Role of Drugs in the Origin of AIDS," Duesberg presented what could be considered the fourth version in a sequence of publicly expressed views about the etiology of AIDS. Back in 1987, Duesberg had started out saying he didn't know what caused AIDS; all he was certain of was that it wasn't HIV. "The charge was then leveled that I was destructive, I was only negative, I was not contributing anything," Duesberg later recalled. But very soon afterward, he began making statements consistent with the immune overload hypothesis. In 1990 his student Bryan Ellison's Policy Review article had expanded this hypothesis (as reworked by Root-Bernstein) and extended it to the other risk groups, formalizing it as the risk-AIDS hypothesis. But in the very course of discussions with Ellison as the article was being written, Duesberg had become increasingly uncomfortable with the generalized focus on any and all forms of risk behavior.
In place of the risk-AIDS hypothesis, Duesberg began to formulate a more parsimonious explanation, the "drug-AIDS hypothesis," which emphasized toxicological causes of AIDS. In a move that signaled his disagreement with some of the other HIV dissidents, such as Sonnabend and Callen, Duesberg dismissed the significance of repeated infections. AIDS was not caused by an infectious agent—not HIV, not CMV, not Epstein-Barr virus, not any combination of the above. Drug consumption—not promiscuous sex—was the lifestyle practice associated with AIDS, Duesberg increasingly became convinced.
Leaving aside the hemophilia and transfusion cases, which had their own explanations, nearly every case of AIDS in the United States and Europe could be attributed to drug abuse.
In his 1992 article in Biomedicine & Pharmacotherapy , Duesberg presented his case in more formal terms. The article included 132 references, mostly to scientific publications but also to popular works by Jad Adams and John Lauritsen. Ever since the turn of the century, Duesberg wrote, "evidence has accumulated that addiction to psychoactive drugs leads to immune suppression and clinical abnormalities similar to AIDS, including lymphopenia, lymphadenopathy, fever, weight loss, septicemia, and increased susceptibility to infections and neurological disorders." These clinical abnormalities became epidemic in the early 1980s as a result of "a massive escalation in the consumption of psychoactive drugs," Duesberg explained, with reference to Justice Department statistics. "Thus the American AIDS epidemic is a subset of the AIDS epidemic." Indeed, only half of the drug-induced immunodeficiency cases receive public notice, due to the hegemony of the HIV hypothesis: "Only the pneumonias, tuberculoses, and dementias of the 50% of American intravenous drug users with HIV are recorded as AIDS, while those of their HIV-negative counterparts are diagnosed by their old names."
How would Duesberg prove a claim that AIDS is caused by drugs? Koch's postulates were not relevant in this case, since they applied only to infectious agents. Duesberg was arguing that the relation between drugs and AIDS was analogous to that between smoking and lung cancer: prolonged and repeated exposure to the toxic substance or substances eventually resulted in disease in some percentage of cases. The problem is that causal relationships of this sort are notoriously difficult to establish, and epidemiologists devote considerable energy to teasing out the various lifestyle risk factors that might confound the relationship (Is the smoker also overweight? Does the smoker drink alcohol?). But Duesberg was not an epidemiologist and had conducted no controlled studies. Nor did his proven expertise in molecular biology or retrovirology have much bearing in this case. Duesberg simply set out to construct a persuasive argument, relying on his background in chemistry and facts at his disposal from his scouring of the published literature.
After quickly reviewing his case for the implausibility of the reigning hypothesis, Duesberg began by noting the "chronological coincidences" between the AIDS and drug epidemics in the United States. Moreover, "drugs and AIDS appear to claim their victims from the
same risk groups." Intravenous drug users comprised about a third of all AIDS patients, Duesberg explained. And about 60 percent of AIDS patients in the United States were male homosexuals, who, according to Duesberg, were disproportionate consumers of drugs. Duesberg reported on a number of studies, including a 1990 survey of "3,916 self-identified American homosexual men, the largest of its kind," which found that 83 percent had used one or more drugs—including poppers, cocaine, amphetamines, and LSD—during the previous six months. Finally, Duesberg turned to another "risk group," healthy antibody positives who had taken "cytocidal DNA chain terminators" such as AZT. "Thus an unknown, but possibly a high percentage of the 30,000 Americans that currently develop AIDS per year have used AZT prior to or after the onset of AIDS."
Even if accepted at face value, these arguments about prevalence of drug use among AIDS risk groups were not particularly weighty in establishing the role of drugs in the causation of AIDS. Indeed, in his own attacks on the HIV hypothesis, Duesberg had frequently invoked the maxim that "correlation is not causation": just because HIV, or drug use, or anything else had been correlated with AIDS, researchers could not necessarily conclude that they had identified a cause. However, AZT presented Duesberg with a particularly convenient target, because by 1992 no one liked the drug very much despite its widespread administration. AZT did not cure AIDS, and it had substantial and potentially dangerous side effects. The initial study that showed it prolonged life in AIDS patients had been ended early when, for ethical reasons, the drug was supplied to study participants getting only a placebo, and some argued that, as a result, there was no clear evidence of the drug's long-term effects. Since 1990 the drug had also been prescribed to asymptomatic HIV positives in hopes of preventing progression to AIDS. But recent studies had been equivocal, suggesting that while the drug might indeed delay the onset of opportunistic infections, it might have no ultimate effect on longevity. By this reading, HIV positives faced a Hobson's choice in the short term—refuse AZT and suffer minor opportunistic infections or take AZT and endure its adverse effects—but arrived at the same place in the end. Another often-criticized but much publicized study had suggested that AZT might be less effective in African-Americans and Latinos than in whites.
To be sure, most doctors continued to prescribe AZT (or chemically related drugs), and public health authorities continued to promote it
as the indicated treatment for HIV positives with abnormally low T-cell counts. But enthusiasm for the drug had waned appreciably. Over the years, particularly in New York, some in the AIDS movement had come out against AZT—including dissenters in the causation controversy, like Ortleb, Lauritsen, Sonnabend, and Callen, as well as some who accepted the HIV hypothesis. Callen—who was well known for the accomplishment of being alive a decade after his AIDS diagnosis—attributed his survival, in large part, to his refusal to take AZT.
In his critique, Duesberg emphasized the drug's side effects: anemia, nausea, muscle atrophy, hepatitis, insomnia, headaches, seizures, and vomiting, among others. Yet although none of these conditions would justify an AIDS diagnosis, Duesberg did not explain his claim (perhaps borrowed from the title of Lauritsen's book, AZT: Poison by Prescription ) that AZT is "AIDS by prescription." Certainly if Duesberg were held to the same rigorous standards of proof that he proposed for the HIV orthodoxy, his argument would have to be found wanting. He had provided no conclusive evidence isolating long-term drug use as the cause of AIDS; he could point to no controlled longitudinal studies of the kind he insisted that the AIDS establishment must perform. And along the way he presented a number of arguments that can only be characterized as specious: "Within 48 weeks on AZT, 172 (56%) out of 308 Australian AIDS patients developed one or more new AIDS diseases, including pneumonia and candidiasis. This indicates that AZT induces AIDS disease within less than 1 year and thus much faster than the 10 years HIV is said to need to cause AIDS." This was like arguing that if a flu sufferer took aspirin, and four hours later her fever returned, then aspirin must cause fever even more rapidly than the influenza virus. Perhaps comments such as these were intended only to goad his critics and were not meant to be taken too seriously. Or perhaps by this point, Duesberg was so embittered by the behavior of his scientific colleagues—who, he believed, had black-balled him, tried to silence him, and succeeded in cutting his funding—that he was willing to employ any rhetorical device at his disposal to cast doubt on the worth of their accomplishments.
By a different calculus, Duesberg might be said to have achieved his objectives with the article in Biomedicine & Pharmacotherapy: he had supplemented what, after all, was his main point—that HIV could not be the cause of AIDS—by proposing an alternative explanation in a legitimate scientific publication. In the past, experts had taunted Duesberg: "Perhaps he would be willing to tell us what, in his view, is
the cause of AIDS and what he would do about it. … It would seem only fair for Professor Duesberg either to come up with an equally strong candidate or to lend his support to eradicating HIV and thus AIDS." Now Duesberg could claim to have met that challenge, and he could return to exerting public pressure on the proponents of the AIDS orthodoxy to prove the official story of AIDS causation.
The HIV Heretics and the "Murdoch Press"
Suddenly, in spring 1992, the causation controversy exploded in the pages of the British press. Between April 26 and May 31, more than twenty articles or opinion pieces on the topic were published in the pages of the Times, the Sunday Times, the Independent, and the Daily Telegraph, or released over the wire by Reuters. The furor was kicked off by the Sunday Times, which—along with the technically separate daily Times, also owned by publishing mogul Rupert Murdoch—had been prone toward headline-grabbing coverage of AIDS. These newspapers had explored the controversial view that the AIDS epidemic might be the unintended by-product of vaccine trials in Africa in the 1950s, which may have exposed vaccine recipients to monkey viruses similar to HIV. They had also fiercely questioned the view that heterosexuals were at risk of AIDS. Now, in a frontpage, headline story, accompanied by a much longer, forty-four hundred-word, double-page spread inside the newspaper as well as a sidebar on Montagnier, science writer Neville Hodgkinson described a "Startling Challenge to Aids Orthodoxy" mounted by "two of the world's experts on viruses," Montagnier and Duesberg.
Both scientists, Hodgkinson reported, "are to challenge the orthodox view that HIV is the exclusive cause of Aids" at an alternative AIDS conference to be held in Amsterdam the following month. Hodgkinson emphasized the shift in Montagnier's position on causation over the years, quoting the French scientist as saying: "We were naive. … We thought this one virus was doing all the destruction. Now we have to understand the other factors in this." And he described the rude reception that Montagnier had received in 1990 when he tried to present his views on cofactors at the International Conference in San Francisco. Hodgkinson quoted one observer: "There was Montagnier, the Jesus of HIV, and they threw him out of the temple."
One of several members of the group profiled by Hodgkinson was
Dr. Kary Mullis, a scientist who in 1983 had invented the technique called polymerase chain reaction that had transformed biotechnology research. (The Financial Times has called PCR "probably the most important development in genetics research since the discovery of gene-splicing in 1973," noting that the market for the technology is likely to be worth $1 billion a year by 1996. In October 1993, Mullis received the Nobel Prize in chemistry for inventing PCR.) Mullis had no expertise in AIDS, but his dissent carried a certain weight, given that his invention had actually been employed to support the orthodox position. Before the invention and distribution of PCR, scientists had been able to find HIV in only one out of every ten thousand to one hundred thousand T cells, raising serious questions about how the virus could be destroying the immune system. But once the same researchers began using PCR, they were able to find the virus in about one percent of T cells—which didn't answer all the questions but at least came closer to doing so. Mullis, however, was not impressed; he told Hodgkinson: "I can't find a single virologist who will give me references which show that HIV is the probable cause of AIDS."
The science editor of the daily Times, Nigel Hawkes, followed up with a shorter article the following day describing the alternative conference to be held in Amsterdam. "Professor Montagnier's presence is likely to give a higher profile to a campaign over AIDS which has been ignored or dismissed by mainstream medical opinion," wrote Hawkes. Meanwhile, Reuters Financial Report noted the financial implication of the Times 's articles for Wellcome Foundation, the British-based parent of Burroughs Wellcome, manufacturer of AZT. Shares of Wellcome stock "took an initial tumble on the article," dropping fifty-two pence. A few days later, the Times 's rival, the Independent, weighed in with a report from Steve Connor, a science correspondent who had coauthored a well-known book about AIDS. Connor quoted Dr. Kenneth Calman, Britain's chief medical officer, who had appeared on television to express his concern that the Times articles might encourage complacency in response to AIDS.
Soon afterward, the Independent published an opposing commentary by William Leith, who compared resistance to Duesberg and Montagnier with the opposition that Darwin and Copernicus had encountered from scientists of their day. "Why do people react so badly to new scientific discoveries?" Leith asked rhetorically. Connor responded with his own op-ed piece, which asked some pointed
questions about what Leith had referred to as "the Duesberg-Montagnier theory." Montagnier's name brought credibility, and the dissenters were understandably anxious to "enroll" him by presenting him as a fellow traveler. But Connor was having none of it. "Readers of several British newspapers could be forgiven for forming the impression that Professor Duesberg has won over a powerful ally," wrote Connor. In fact, Connor explained, Montagnier would be attending the alternative conference in order to oppose Duesberg. He quoted Montagnier's current opinion of Duesberg: "He's wrong because he doesn't take all the data into account, whether deliberately or not. I will go to the conference to prove Duesberg is wrong."
Connor argued that the Times 's misrepresentation of Montagnier's relationship to the HIV controversy was typical of an article that devoted two pages to Duesberg "but largely ignored the welter of evidence against his claim." Malcolm Dean, writing in the "News & Comment" section of the British medical journal Lancet, made a similar point in an article on "AIDS and the Murdoch Press." Decrying the Times 's "deep Conservative bias which the editor desperately tries to conceal by anti-establishment campaigns," Dean argued that "of course sceptics should be given space, but iconoclasts should be pushed as hard as establishment figures to justify their assertions."
Mavericks and High-Flyers
Darwin, Copernicus, Galileo—such names are often invoked to enhance the credibility of anti-establishment figures in science. These comparisons put a premium on challenge and innovation while equating "normal" science with dogma, superstition, and intellectual stagnation. In fact, the heroic imagery of revolutionary science appealed to many of the protagonists in the causation controversy, constituting an important dimension of what Pierre Bourdieu would call their scientific habitus—the particular set of dispositions and "generative schemes of perception, appreciation and action" that engender "the choice of objects, the solution of problems, and the evaluation of solutions."
Duesberg himself was a good example—a brilliant high-achiever, with a history of swimming against the current, a researcher who disdained the mediocrity that he equated with establishment science. The peer review process that governed the scientific world punished the "Mozarts" while rewarding the "Salieris," Duesberg explained, leaving
little doubt as to how he would classify himself. Peer review was "good for technicians, but not for innovation"; it constituted the "stabilization of mediocrity."
For Root-Bernstein—at twenty-seven the second youngest to receive a MacArthur "genius grant" in the 1981 cohort of winners—the $144,000 award meant that he could abandon a "restricting" and "boring" postdoctoral fellowship and conduct a study of scientific creactivity. One reviewer of Root-Bernstein's book Discovering noted its clear sympathies: "Root-Bernstein's characters venture the heretical notion that the clustered, prize-ridden, hierarchical culture of modern science may actually impede important discovery. … What do today's superstar academic-administrator-researchers really think of seminal investigators like Mendel, a monk who discovered the laws of heredity in a monastery garden without federal grants …? Would establishment science even listen to such outside maverick voices today?"
Kary Mullis, called by Time magazine the "hippie-holdout biochemist" and the "Last of the Great Tinkerers," says he conceived of the breakthrough technique of PCR "while winding through the mountains of Northern California" at midnight in his Honda Civic. Claiming to read widely in cosmology, mysticism, mathematics, virology, chemistry, and artificial intelligence, Mullis published an article in Nature on "The Cosmological Significance of Time Reversal" while a graduate student in biochemistry at the University of California at Berkeley. "If you're too establishment-oriented, you're not likely to come up with something really original," Mullis told the Los Angeles Times . In 1993, when he won the Nobel Prize, Mullis was pictured on the front page of the local San Diego Union-Tribune in a wetsuit, surfboard under one arm; reporters marveled at the collection of giant inflatable penguins that adorned his living room.
Mavericks, innovators, individualists—these were people who were unafraid to cross disciplinary boundaries and venture outside of their areas of expertise. And they shared a critical view—call it a loathing—of contemporary "big science" and the way it squelched imaginative efforts. "When a new theory deviates from that held by the majority, it is labeled 'controversial' rather than 'original,'" Duesberg wrote in a commentary piece in The Scientist, with specific reference to Montagnier, Root-Bernstein, and himself; "and the 'controversial' label is tantamount to a death sentence, manifested by non-invitations to meetings, non-citations in the literature, non-nominations for awards, and non-funding of research grants."
Gathering of the Tribes
Sponsored by a Dutch organization called the Foundation for Alternative AIDS Research, which stressed "freedom of information" and "freedom of thought," the alternative conference promised by the Sunday Times took place from May 14 to 16, 1992. Many of the key HIV dissenters were there: Michael Callen, Joseph Sonnabend, John Lauritsen, Joan McKenna, Gordon Stewart, Robert Root-Bernstein, Joan Shenton, Celia Farber, Jad Adams—along with, of course, the featured attractions, Duesberg and Montagnier. Other supporters of alternative positions came from a number of countries on the Continent, including Switzerland, Belgium, and the Netherlands. Representatives of the orthodox position were also in attendance, including three Dutch researchers, Roel Coutinho, Jaap Goudsmit, and Frank Miedema. In all, about two hundred people showed up for the event.
A Reuters report quoted the Secretary of Britain's Medical Research Council, who denounced the claims presented at the alternative conference as "a lethal cocktail of untruth and ignorance." But Nigel Hawkes, writing from Amsterdam for the Times of London, framed the issue as one of freedom of belief versus the suppression of heresy. He led off with: "In an old church in Amsterdam once used by religious liberals escaping persecution, a group of free-thinkers yesterday met to denounce the authorised version of Aids. …" Hawkes noted that "Montagnier insisted that the virus was a necessary part" of the spread of the epidemic, but he presented Montagnier as sympathetic to the dissenters: "'Dogmatism is a deadly sin in the process of science,' Professor Montagnier concluded. This was clear evidence, some might say, that he backed the efforts of the alternative Aids group to take a fresh look at a disease that has been spreading for a decade without a cure or a clear understanding of how it functions being found."
The considerable debate in the British press caused some Canadian publications to pick up the issue. The magazine Macleans published a long article on the Amsterdam conference, and the Toronto Star ran a story describing what it called "The New AIDS Controversy." But in the United States, home to most of the prominent HIV heretics, the alternative conference was almost entirely ignored by the mainstream press. National Public Radio's Weekend Edition ran a brief and not terribly illuminating report picked up from a correspondent for the
Canadian Broadcasting Corporation. But only readers of the gay press would have been likely to know significant details or to have followed the specific controversy concerning the role of Montagnier.
Initially, writers in gay publications followed the lead of the Sunday Times in assuming that Montagnier had defected to the dissident camp. An article in the New York-based magazine QW , entitled "HIV Does Not Cause AIDS, Virus Discoverer Claims," commented: "Although the multifactorial approach is not new, it is surprising coming from someone who is considered relatively conservative and has championed the traditional 'HIV causes AIDS' theory." Similarly, Neenyah Ostrom's article in the Native was headlined: "Montagnier: HIV Is Not the Cause," while the San Francisco Sentinel reported that "other respected AIDS experts have begun to agree with Duesberg, most notably, Luc Montagnier. …"
Claims such as these apparently provoked consternation at San Francisco's Project Inform. One of the most authoritative voices on treatment issues within the AIDS movement, Project Inform had taken many anti-establishment stands. But on the question of causation, the organization stood squarely in the mainstream. Indeed, Executive Director Martin Delaney had become friends with Robert Gallo—initially out of the pragmatic position that it was more useful to the cause of AIDS research to have Gallo on board, but ultimately out of genuine respect for the researcher's talents and a belief that Gallo was being unfairly treated in the controversy surrounding the discovery of HIV. Delaney immediately wrote to Montagnier at the Pasteur Institute to express concern about the Times 's implication of an alliance between Montagnier and Duesberg and to request clarification of his views. Just before leaving for the alternative conference, Montagnier sent off a letter in response, which Delaney released to the press.
In the letter, Montagnier described the Sunday Times article as "misleading since it mixed a correct account of my interview with anti-HIV non scientific theories." However, "as you may recall from our meeting in 1990, my permanent position has been to keep an open mind and not to neglect any facts." Montagnier went on to reiterate his belief that mycoplasma may serve as cofactors, and that various indirect mechanisms—particularly one called "apoptosis" or "programmed cell death"—may be involved in T-cell depletion. But he stressed: "This is just opposite to the view that AIDS is not caused by HIV and is not a transmissible disease."
Project Inform Stakes its Claims
The seriousness with which Project Inform took the resurgence of interest in the causation controversy was indicated by the publication in early June of a six-page "Discussion Paper" devoted entirely to the topic. The report began by blasting the media for their irresponsibility and sensationalism. Why do reporters love the HIV dissenters? Why have they confused Montagnier's position with Duesberg's, despite Montagnier's own disavowals? "Apparently because it makes a good story—'Conventional Wisdom Is Wrong! Top Scientists in Error Ten Years! Secrets! Coverup! Big Business, Big Science Collusion!' … Such is the sorry state of AIDS reporting in some circles today."
Focusing on four groups opposing the HIV hypothesis—the New York Native, Spin magazine, assorted journalists, and certain scientists—Project Inform was at pains to question the credibility of each and to uncover motivations for adopting heretical stances. Accusing the Native of a "supermarket tabloid" mentality, the report described the newspaper as "driven not by any scientific data but by a seething hatred of Dr. Robert Gallo. …" And for writers at Spin , as well as "a few journalists" writing for publications like the Times of London and the Atlantic Monthly , the apparent motivations were "a generic distrust of authority and government science."
In considering the fourth, crucial group of HIV dissenters—the scientists—Project Inform's report similarly emphasized the issue of credibility. Root-Bernstein "works in a field not directly related to AIDS" and "has not conducted or published any AIDS research other than editorials," yet "Spin calls him 'one of the leading AIDS researchers in the US.'" Kary Mullis, while "obviously a serious scientist," was similarly "an outsider to AIDS research"; furthermore, his PCR test "has if anything, helped to bolster the case for HIV." Of all the heretical scientists, only Sonnabend "is professionally involved with AIDS," but "primarily as a clinician": "While Dr. Sonnabend has earned respect in many ways, his arguments against HIV are no more valid than the others."
The case against the credibility of Peter Duesberg was given more extended treatment. Project Inform explicitly posed the crucial question: "Is Peter Duesberg an 'AIDS expert'? That depends on the definition of 'expert.'" The report reviewed the evidence in terms that mirrored Gallo's characterization of his colleague: Duesberg had never
conducted laboratory, clinical, or epidemiological research on AIDS or HIV. He was trained in chemistry, not the biological sciences. He had "no known professional expertise regarding the immune system, was not an expert in the study of human viruses or retroviruses, nor in human disease in general (except for cancer)." True, he once mapped the genetic code of a retrovirus, but that work "bears little direct connection to AIDS."
In focusing on formal credentials, Project Inform walked a fine line. This, after all, was a grassroots organization staffed by self-educated AIDS experts; its executive director, before the epidemic came along, had been a business consultant. A big part of Project Inform's work involved disseminating highly technical knowledge about AIDS to laypeople in order to create what might be called a mass-based expertise. In its reckoning of the tokens of expertise, Project Inform was not about to argue that academic degrees or journal publications are everything. Lacking the right credentials, Peter Duesberg could still be considered an AIDS expert of sorts—but not in a way that would make him stand out from the crowd: "Perhaps his most relevant work is that he has studied the medical literature on AIDS (as have thousands of patients, physicians, and activists), and this qualifies as a form of expertise." But "Duesberg's supporters and the media spread misinformation when they present him as an 'AIDS researcher' in the sense that phrase is usually meant." His published writings on AIDS were "simply editorials."
Project Inform noted that there was a "legitimate" scientific question that had been "lost in the fog" generated by media fascination with Duesberg and other dissenters: How does HIV cause AIDS? Following the lead of Gallo and others, the report emphasized that pathogenesis was separate from etiology; while part one of the report was entitled "Is HIV the Cause of AIDS?" part two was called "How Does HIV Cause AIDS?" Here Project Inform adopted an agnostic position, informing its readers about a variety of hypotheses, including "specific co-factors," "general infectious co-factors," "superantigens," "apoptosis" (Montagnier's position), "autoimmunity," "overactivation," and "antigen diversity threshold." Project Inform's point was that speculation about these pathogenetic mechanisms was an entirely mainstream endeavor and had been since the beginning. "Few if any researchers," the report argued, "ever claimed that AIDS was solely the result of HIV killing [helper T] cells. It was the media who spread that view, apparently to simplify AIDS for the public."
While reviewing the various positions on etiology and pathogenesis, the report also took time to blast Duesberg's alternative causal hypothesis: "By linking AIDS to behavior, rather than a virus, Duesberg paints all but the 'innocent' victims of AIDS as promiscuous drug abusers. … When such views are expressed by fundamentalists and right wing politicians, they are routinely and correctly branded as homophobia and racism . Such well-known bigots as Congressman William Dannemeyer today quote Duesberg as the scientific source of their views." Against these charges, the report reminded readers of a "simple truth" known by "anyone in a community hard hit by AIDS"—that "some who have died did have histories of promiscuity and drug abuse, but many, many others did not."
Left and Right
By labeling Duesberg homophobic, and by associating him with political enemies on the right, Project Inform sought to annul any credibility that Duesberg might enjoy in gay and lesbian communities. Duesberg himself, however, assiduously rejected any taint of homophobia: "In reality I've paid more … to them than … most of my fellow AIDS researchers, who're making millions of dollars by killing homosexuals by the hundreds of thousands with AZT. … It's actually absurd that I'm being labeled the homophobe, when I might in fact have found the real cause of their problem. …" Whatever Duesberg's beliefs, it is certainly the case that the political configurations in the Duesberg controversy have been more complex than simple labels could suggest. For example, some left-wing commentators have supported Duesberg out of a principled objection to monocausal disease models. "Ruling classes embraced modern medicine because the germ theory blamed disease on invisible microbes and not hazardous conditions," according to one pro-Duesberg magazine article from 1989. Yet the appeal of Duesberg's views to conservatives—certainly including those with little sympathy for the gay movement—cannot be denied.
Charles Thomas, the organizer of the Group for the Scientific Reappraisal, has described himself as "libertarian" and claimed that he left Harvard in disgust because the universities had become "totally corrupted by affirmative action, political correctness, the whole nine yards." He criticized the AIDS activist movement as one of "victimology": by portraying AIDS as an "act of God," rather than the consequence
of behavior, homosexuals generated sympathy and government funding. Philip Johnson, the Berkeley law professor on the group's steering committee, has also been known for his conservative views. Bryan Ellison made no bones about why he sought to promote Duesberg in the Heritage Foundation's Policy Review , as well as in California Political Review , a journal that has also featured articles about "Hollywood's leftward tilt" and Republican California Governor Pete Wilson's "liberal surrender." Tom Bethell, a columnist who has written in support of Duesberg in various publications, is well known for his right-wing positions, which have included endorsement of such political figures as Patrick Buchanan. Bethell's columns in the Los Angeles Times include one entitled "We May Regret Going Along with This: The Gay-Rights Agenda Precludes Any Public Doubts." Elsewhere he has expressed sympathy for homosexual "recovery" organizations (which encourage gays and lesbians to become straight).
The "Vietnam Syndrome"
Project Inform concluded its commentary with some speculation about Duesberg's motives for continuing to pursue the controversy. Portraying Duesberg as "a propagandist, not a reasoning scientist," Project Inform's report noted the incendiary quality of Duesberg's claims when he labeled AZT as "iatrogenic genocide": "He presses the hot buttons of genocide, distrust of authority, fear of doctors, and suspicion of business—all in two carefully chosen words." Why would Duesberg be doing this? What could he possibly stand to gain? And doesn't the fact that he is being silenced by the scientific establishment mean that the AIDS movement should support him? Project Inform had its analysis at the ready: "Having gone out on this limb, personally and professionally, he got stuck there and is hanging on with great tenacity. It is true that the scientific mainstream sometimes (but rarely) makes a giant error and clings stubbornly to it, it is far more common that individual scientists do so."
Had Duesberg—along with other dissenters whose credibility was on the line, like Sonnabend and Root-Bernstein—simply gone too far to turn back? Had they become trapped by the nature of their prior investments? Even Bryan Ellison acknowledged, in describing his mentor's progress: "He slowly got more and more into it, and now, what's he going to do, back out?" Yet such arguments cut both ways.
Thomas Ryan, a supporter of Duesberg writing in the gay magazine Christopher Street , used the metaphor of the U.S. government's pursuit of victory in Vietnam to describe the ongoing commitment of the establishment to the HIV hypothesis: they simply had invested too heavily to pull out. And this could be said not just of the scientists, whose professional reputations were at stake, but of the wider "AIDS community" that had fashioned its very identity in response to the ramifications of the HIV hypothesis. "If anything positive has resulted from the AIDS crisis, it is the solidarity it has inspired in the gay community, and nothing has so threatened that uity as the HIV debate," wrote Ryan. Or as Drew Hopkins, another Duesberg sympathizer also writing in Christopher Street , observed: "If HIV is not the cause, the entire body of AIDS advocacy is undone from its foundation. Every issue must be re-examined from a new, uncertain perspective. Such a confusing period would also generate a dangerous vulnerability. As AIDS has become a more and more political issue, it would take very little for a Pat Robertson, Jesse Helms, or William Dannemeyer to seize the day, using the period of reassessment on the part of the AIDS community to conduct still more virulent campaigns of fear and hatred."
"AIDS Without HIV"
The wave of publicity that seemed to propel Duesberg forward throughout 1992 picked up additional momentum in July, with the opening of the Eighth International AIDS Conference. Convening in Amsterdam like its "alternative" predecessor of a few months before, the conference was sidetracked by breathless reports in the mass media of an "epidemic" of cases of "AIDS" in people who tested negative for antibodies to both HIV-1 and HIV-2. "The patients are sick or dying, and most of them have risk factors," wrote Newsweek , describing a dozen such cases. "What they don't have is HIV." Perhaps a new virus was at work, a possibility that seemed to gain credibility in the media due to the coincidental report by a southern California scientist of the isolation of an apparently new retrovirus in AIDS patients. Or perhaps there were other routes that led to conditions like AIDS. Newsweek 's speculations must have inspired intense flashes of déjà vu in those familiar with the debates about causes of AIDS that had been enacted a long decade earlier: "Dr. Alvin Friedman-Kien of the New York University Medical Center notes that
gay men and IV drug users contract numerous infections, from gonorrhea to herpes and hepatitis. Some ostensible AIDS cases may simply reflect the immune-suppressing effects of common germs or of poor nutrition, he says."
Besieged by reporters, scientists, and activists, James Curran, the head of the CDC's AIDS office, was forced to address the new syndrome at a heated conference session. Curran acknowledged that the CDC had been tracking such cases, but insisted, "These are not cases of AIDS"; he then made the circular argument—which Duesberg must have appreciated—that a definition of AIDS requires the presence of HIV. Duesberg wasted little time sending in a letter to Science , offering to provide to anyone who was interested "a list of references to more than 800 HIV-free immunodeficiencies and AIDS-defining diseases in all major American and European risk groups," along with references to "more than 2,200 HIV-free African AIDS cases." Rather than rushing to conclusions about any new virus, Duesberg advised, Science should focus attention on alternative explanations "that could resolve the growing paradoxes of the virus-AIDS hypothesis."
Only days after the first reports of the mysterious cases, this newest controversy framed a debate in the pages of the Los Angeles Times about the arguments of Peter Duesberg. Steve Heimoff wrote one of the two, side-by-side, opposing op-ed pieces, leading off with the observation that reports of "AIDS without HIV" would "appear to signal at least partial, temporary vindication" of the Berkeley scientist. Describing Duesberg as "the unofficial leader of the revisionists," "an international star of virology long before anyone heard of AIDS," and "not just another conspiratorialist," Heimoff reported that many of his arguments "have the ring of common sense." It would seem that "there are now three legitimately contending theories regarding the causes of AIDS," Heimoff said: the official CDC theory, Montagnier's cofactor theory, and Duesberg's. Heimoff concluded: "If there is even a remote chance that Duesberg is correct—and the latest reports increase that possibility—then the powers that be must leap into action."
"Just because the Establishment has been wrong so often doesn't necessarily make all of its critics right," Duesberg's old foe Michael Fumento responded in the accompanying piece. "Duesberg's methodology in determining that HIV doesn't cause AIDS is less science than a game in which he tells his opponents to go into a round room and sit in a corner." Turning to Duesberg's alternative hypothesis,
Fumento noted that the theory failed to explain AIDS in Africa, where neither AZT nor recreational drugs were in significant use. This prompted Duesberg and Ellison to respond, in a letter to the editor, that the official WHO statistics "reveal a tiny African AIDS epidemic" despite large numbers of HIV positives. They complained that Fumento also pointed to "media-publicized cases of ordinary people developing AIDS" but that he failed to mention that "Ali Gertz used cocaine, Ryan White suffered from fatal hemophilia, Paul Gann had traumatic heart surgery, Kimberly Bergalis used AZT, and Magic Johnson is symptom-free."
In the gay and lesbian press, responses to the "AIDS without HIV" flap were generally dismissive. Many denounced the "media circus" or "media feeding frenzies" that seemed predictably to ensue when too many reporters knowing too little about AIDS found themselves together in one place with too little hard news to write about. Martin Delaney, writing in his regular column in the Advocate , insisted on the "clear point" that "these events have nothing to do with the so-called Duesberg theory," and he warned that Duesberg's "supporters will no doubt seize on the new information as an assault on the role of HIV."
On the far end of the spectrum, Chuck Ortleb penned an editorial for the New York Native , entitled "Honey, I Blew Up the HIV Paradigm." Attacking the CDC for "promoting the religious belief that HIV is the cause of AIDS," Ortleb pushed the Native 's current theory, that AIDS and the chronic fatigue syndrome were "variants of the same disease": "If the C.D.C. wants to know all cases of HIV-negative AIDS, we hereby report to them 13 million cases: the estimate of the number of people in the U.S. with Chronic Fatigue Syndrome [CFS]." While the CDC was unlikely to have been impressed by Ortleb's statistics, indirect support for the Native 's publisher arrived from an unlikely source, when Newsweek published a follow-up story on "AIDS without HIV" that played up the chronic fatigue angle. "As more cases come to light, it's becoming clear that the newly defined syndrome has as much in common with CFS as it does with AIDS," said the Newsweek reporter, Geoffrey Cowley.
Following on Newsweek 's lead, Time magazine published a cover story entitled "Invincible AIDS," which suggested that the global fight against the epidemic was in disarray. But over the next few months, the AIDS establishment struggled to put its house back in order. In August the CDC convened a special panel to review all cases of "AIDS without HIV" that had been reported or that investigators
had been able to dig out of medical records. The panel dismissed as flawed the reports describing a new virus. But they agreed that a syndrome did exist—the CDC had dubbed it "idiopathic CD4+ T-lymphocytopenia" (ICL) to describe the depletion of helper T cells by an unknown cause —though only thirty confirmed cases could be found in the United States. Moreover, in contrast to the earliest reports, it now appeared that more than half the ICL patients reported none of the AIDS risk factors. As compared with AIDS cases, people with ICL were more likely to be older than fifty, more likely to be white, and more likely to be female.
The consensus of panel members was that different patients were immune-suppressed for different reasons. Most likely there had always been small numbers of such cases, but they had never before come to national attention because there was little medical emphasis on T-cell testing. "Only in the last three to four years has CD4 [helper T-cell] testing become a mass industry," commented Martin Hirsch of Harvard Medical School. The following month, the WHO reported similar findings based on a review of cases of ICL from around the world.
The Dynamics of Closure: Whither the Controversy? (1992–1995)
The Definitive Study?
Overshadowed by the news about "AIDS without HIV" were other research findings that augured less favorably for the future success of the HIV dissenters, particularly Duesberg. First, over the summer of 1992, two groups of researchers reported on the latest advances in isolating HIV from T cells using PCR technology. Instead of finding the virus in one out of every ten thousand or one hundred thousand cells, scientists were now succeeding in finding the virus in one out of every forty to two hundred cells. The following January, Dr. Ashley Haase of the University of Minnesota and other researchers reported on their refinement of PCR called "PCR in situ," which allowed them to discover HIV in 10 to 30 percent of T cells and in high percentages of other cells as well. These findings, the authors explained, were "consistent with the emerging view that HIV infection per se could contribute substantially to depletion of immune cells in AIDS."
Further relevant data were published in March, when two groups
of researchers, one led by Haase and the other by Anthony Fauci, described finding "massive covert infection" of lymphoid cells in the spleen, tonsils, adenoids, and lymph nodes during the early stages of HIV infection—ten times more virus than could be detected in blood samples at that stage of illness. "These developments," wrote Nature editor John Maddox in the Times of London, "convincingly give the lie to Duesberg's only cogent criticism of the conventional view that it is difficult to recover virus from the helper T-cells circulating in the blood." Maddox continued: "Now it seems probable that these vital components of the immune system are damaged and perhaps killed off in the relative obscurity of the lymph nodes and the other organs of the immune system."
Another piece of news (which received little notice beyond a brief report in a New York Times article devoted mainly to other topics) arrived in a presentation at the International AIDS Conference that was designed specifically to prove Duesberg wrong. The report was by Kevin Craib and other researchers with the Vancouver Lymphadenopathy-AIDS Study, one of the principal cohort studies that had been tracking HIV-negative and HIV-positive gay men for nearly a decade. The study's authors noted Duesberg's argument that no controlled study had been conducted that could truly distinguish between lifestyle risk factors and HIV infection as possible causes of AIDS. "The purpose of this analysis," wrote Craib and his associates, "was to conduct just such a controlled analysis within a cohort of homosexual men."
Looking back over their accumulated data, Craib and his coauthors investigated the incidence of AIDS-defining illnesses and changes in T-cell counts over time and tried to relate those clinical developments to HIV status, to exposure to psychoactive drugs, and to sexual behavior. They found that half of the 350 HIV-negative men in the study reported using psychoactive drugs. And about a quarter of them reported having been the receptive partner in anal intercourse with "casual partners." But despite these high incidences of (hypothesized) risk behavior, there were no signs of immune dysfunction in the seronegative group—no AIDS-defining illnesses and no drop in T-cell counts. Of 134 AIDS-defining illnesses in the full cohort, "every single one occurred in men with pre-existing evidence of HIV infection." Cofactors might determine which HIV positives contract which (if any) opportunistic infections, the authors concluded; "but claims that AIDS is caused by other exposures and not by HIV are clearly not borne out by these data."
The Berkeley epidemiologist Warren Winkelstein had already shown Duesberg unpublished figures, derived from the San Francisco Men's Health Study, that supported similar conclusions. Duesberg, however, insisted that unpublished data simply didn't count in the world of science, and he refused to acknowledge Winkelstein's findings unless they appeared in a peer-reviewed journal. Winkelstein maintained, in response, that these were really nonfindings and that scientists weren't generally in the business of publishing nonassociations. But in the end Winkelstein was induced to answer to his nemesis; and in March 1993, an immunologist named Michael Ascher, along with Winkelstein and other colleagues, published a commentary in Nature entitled "Does Drug Use Cause AIDS?" The article appeared the same week as the formal publication of Craib's study in Lancet —a double whammy that attracted the media attention that Craib's conference presentation had failed to elicit.
Ascher and his colleagues assembled a point-by-point argument that seemed intent on addressing every objection that Duesberg had ever voiced or might conceivably muster in the future. It was a strong piece of science and very much a political document, one which acknowledged as its motivation "the wide publicity attracted by [Duesberg's] assertion." Ascher and his colleagues reviewed the San Francisco Men's Health Study data for 1,027 study subjects over ninety-six months. According to interviews performed at the beginning of the study back in 1984, the 812 gay or bisexual men and the 215 straight men had used cocaine, marijuana, and amphetamines in roughly the same percentages during the two years prior to recruitment for the study. (For example, 36 percent of homosexuals/bisexuals and 39 percent of heterosexuals had reported using marijuana once a week or more.) Since 26 percent of the gay or bisexual men had been diagnosed with AIDS indicator diseases over the course of the study, one would therefore expect that roughly the same percentage of the heterosexuals would also have AIDS diseases, if drug use were indeed the cause. But in fact, there were no cases of AIDS indicator diseases in the heterosexual group.
Noting that "the clinical case definition of AIDS has been criticized as having subjective features and low specificity," the authors also presented data examining the relationship between T-cell counts over time, drug use, and one's status as antibody positive or negative. T-cell counts, after all, were "the primary pathognomonic feature of AIDS"; they were the best indicator of the health or impairment of the
immune system in people at risk of AIDS. The results were striking: The average numbers of T cells (per cubic millimeter) for the seropositives declined steadily from about seven hundred in 1984 to about four hundred in 1992, regardless of extent of drug use. But the average numbers for the seronegatives stayed the same, at one thousand to twelve hundred T cells—although ironically, the heavy and moderate drug-using seronegatives actually had slightly higher T-cell counts than the seronegative abstainers. This was a surprising finding, but it hardly helped Duesberg's case. The researchers concluded with their own challenge for their adversary: "The energies of Duesberg and his followers could better be applied to unraveling the enigmatic mechanism of the HIV pathogenesis of AIDS."
The Terms of the Debate
One of the dissenters' strongest arguments, which made an appearance in practically every published statement that any of them had made over the course of more than eight years, was that closure had been reached prematurely in 1984. A "probable cause" had been identified that was soon taken to be "the cause," yet no one bothered to prove it definitively. Instead, the world simply acted on what it took to be the truth. By the mid-1990s, however—particularly as a result of data from long-running cohort studies—the state of the evidence looked rather different. Indeed, one might even argue that the dissenters' challenge and the ensuing controversy had served to promote clearer argumentation on behalf of the HIV hypothesis. In that sense, ironically, the dissenters may have helped to reinforce the dominance of the position they opposed.
Does this mean that the end of the controversy was in sight? That would have been an overly hasty conclusion, and one that ignored recognized pitfalls along the path to closure in scientific controversies. In their consideration of the question of how scientific controversies end, H. Tristram Engelhardt and Arthur L. Caplan have noted the danger in assuming that complex disputes can be adjudicated through straightforward, rational means. The notion that a controversy can be "settled" presupposes prior agreement on "(1) how to acquire evidence relevant to the dispute and (2) how to reason with the evidence in order to reach a rationally defensible conclusion that will resolve the controversy." In fact, differing perceptions of what "the controversy" is and what sort of evidence might "settle" it are themselves often stakes in a controversy. This is all the more likely to be true,
Engelhardt and Caplan have observed, when "stakeholders in the debate belong to … different communities with different appreciations of the evidence at stake" or to "competing social groups" with opposing political and ethical agendas.
How does one prove disease causation? Without agreement on this basic question, there was little chance of consensus about the relation of HIV to AIDS. In the early 1980s, many researchers, including even Gallo, seemed to have Koch's postulates at least generally in mind as they sought to isolate the virus, to induce the syndrome in primates, and to trace transmission of AIDS through infected blood products (see chapter 2). But when challenged by Duesberg, researchers argued that Koch's postulates were rarely satisfied in practice, especially for viruses; and they pointed to well-known examples.
As Duesberg pressed his case, both sides moved toward the position that specific epidemiological evidence—especially controlled longitudinal data—is what could settle the question. But where epidemiologists such as Winkelstein insisted that the existing data from cohort studies already provided a definitive answer, Duesberg maintained that a meaningful cohort study had not yet been performed: The existing studies were created with the goal of studying the progression of "HIV disease." They were not set up to determine what causes AIDS, let alone to study drugs as a possible cause, and, Duesberg claimed, the data that had been collected about participants' drug use were superficial and inadequate. Neither Winkelstein nor the Vancouver group asked about drug use occurring as far back as ten years prior to entry into the study; nor had any of the cohort studies included blood tests for drugs, which Duesberg claimed were necessary to verify if the study participants were answering truthfully. From the perspective of Duesberg and his allies, these aspects of data collection rendered the cohort studies worthless in adjudicating between causal hypotheses. Duesberg's deconstruction of the cohort studies demonstrated clearly what science studies scholars have repeatedly argued: in situations of controversy, experiments alone cannot be expected to "settle" the dispute. "The problem with experiments," according to Harry Collins and Trevor Pinch, "is that they tell you nothing unless they are competently done, but in controversial science no-one can agree on a criterion of competence." Moreover, any experiment is—admittedly—an artificial stand-in for real-world conditions. Does the experimental situation adequately represent and capture reality? Nothing inherent in the experiment itself forces the observer to accept it as such.
Both sides remained convinced of the validity of their claims; each
side saw the other as dogmatically defending its position by means of a constant renegotiation of the rules. From Duesberg's standpoint, the defenders of orthodoxy were always "moving the goalposts" whenever its predictions were proved false; from the vantage point of the dominant position, the dissenters were forever cooking up newer and stricter criteria of proof that their opponents were then expected to meet. "Like a child who questions every answer with another 'why,' he plays a game which will never end until he says it is over," was how Martin Delaney characterized Duesberg's methodology in late 1992. But perhaps the real mistake was to imagine that there is one "scientific method" or set of "rules of evidence" upon which everyone could unproblematically agree. Indeed, if the controversy has demonstrated anything, it is that scientific "rules of the road" like Koch's postulates or epidemiological cohort data, far from being unchallengeable benchmarks, may be as subject to interpretation and debate as the empirical phenomena they are invoked to explain.
Most likely there is no scientific test that would settle the causation controversy to the satisfaction of all sides. A different sort of proof probably would spell the end of the controversy, however: if the AIDS establishment were to succeed in finding an impressively successful antiviral drug or vaccine, it is unlikely that anyone would continue to pay much attention to the dissidents. They would simply fade from the scene. This, however, is not entirely logical, for, as René Dubos has argued, it can be dangerous to infer medical etiology "backwards" from treatment effectiveness: "While drenching with water may help in putting out a blaze, few are the cases in which fire has its origin in a lack of water." Yet at its root the support for the dissenters stems precisely from disappointment with the establishment's lack of therapeutic success, as the dissenters themselves have been acutely aware. Michael Callen told a Canadian television program in 1989: "It seems to me that if … you've got a chemical that is anti-retroviral … and you give it to people who have a disease that you claim is caused by a retrovirus and they don't get better, that would tend to suggest—at a minimum—that something a lot more complicated than having or not having HIV is going on." The more time that has passed without a cure being discovered, the more persuasive has been the argument that the AIDS establishment has "produced nothing" and—by extension—their etiological hypothesis must be bankrupt. From a logical standpoint, this, of course, follows even less obviously than the converse claim that the existence of a successful treatment would verify the
causal hypothesis. But the argument has a rhetorical power that cannot be denied. "As long as there's no cure, this will lurk," Robert Gallo reflected in 1994.
Meanwhile, the struggle has gone on, and the HIV dissenters have continued to make the news. By now several of the principals have told their stories in book-length detail. Root-Bernstein's Rethinking AIDS: The Tragic Cost of Premature Consensus , published by Free Press, weighed in at 512 pages and included 100 pages of notes. It reviewed the anomalies in the HIV hypothesis, discussed a range of multifactorial theories of AIDS, and delved deeply into theories of autoimmune mechanisms. Lauritsen's The AIDS War: Propaganda, Profiteering and Genocide from the Medical-Industrial Complex , a reprinting of many of his articles, likewise ran nearly 500 pages. Ellison and Duesberg encountered more obstacles with their book, which was accepted but then dropped by two different publishers. By 1994 the book fell victim to a bitter feud that erupted between the two authors and led to a parting of the ways. Working alone, Duesberg finally published the book Inventing the AIDS Virus in 1996. In addition to 463 pages of new text, the book included reprints of several of Duesberg's scientific articles; it also featured a foreword by Kary Mullis. In this extensive review for the general reader, Duesberg summarized the views he had been putting forward for nearly a decade—not only on the HIV hypothesis and the drug-AIDS hypothesis, but on the status of the field of virology and the politics of science in general.
The ranks of the dissenters were depleted in December 1993 by the death of Michael Callen, who had lived with AIDS for nearly twelve years and played a central role in a range of activist projects. Other dissenters have continued to engage public attention. Notable occasions have included the appearances by Duesberg, Kary Mullis, and Philip Johnson at a special panel of the annual meeting of the Pacific Division of the American Academy for the Advancement of Science; a Florida physician's public self-injection with apparently HIV-infected blood to draw attention to "the greatest scam ever perpetrated"; and a freshman Republican Congressman's attempt to force government scientists at the NIH and CDC to consider the view that HIV does not cause AIDS.
Perhaps most noteworthy, however, was a high-profile "Special News Report" called "The Duesberg Phenomenon," published in Science in late 1994 and taking up an extraordinary eight pages of the
premier journal. "Because the Duesberg phenomenon has not gone away and may be growing," wrote Jon Cohen, the AIDS reporter for Science and the author of the news report, "Science has decided this was a good time to examine Duesberg's main claims." Cohen's strategy was to tackle Duesberg's arguments head-on; in a series of sidebars, he considered each of the critical test cases. Although scrupulous in presenting Duesberg's views, the article suggested that Duesberg was wrong on all counts: being HIV positive was the key variable associated with HIV-related illness for hemophiliacs; Koch's third postulate had been satisfied by the accidental infection of three laboratory workers, all of whom developed symptoms of immune suppression prior to taking any antiviral drugs; and large, recent studies of extended AZT use showed no evidence that the drug caused AIDS. Not surprisingly, this intervention ignited yet another wave of publicity: though Cohen may have intended exactly otherwise, his article propelled the Duesberg phenomenon onward. Indeed, a long article in The Scientist published in March 1995, which led off with the special report in Science , was entitled "A Controversy That Will Not Die: The Role of HIV in Causing AIDS."
Years after the publication of his article in Cancer Research , Peter Duesberg has settled in for the long haul. The HIV controversy has become his life; his office on the Berkeley campus is the war room of a campaign waged simultaneously on multiple fronts. Duesberg maintains a frenetic pace, juggling reporters and visitors between poring over the latest AIDS publications and preparing his latest rebuttals. Though he might not agree with much that Anthony Fauci has to say, he would doubtless concur with one prediction that the NIH scientist made back in 1989: "I am probably going to be answering Peter Duesberg for the rest of my life."
Causation and Credibility
The story told in part one—the story of the early search for the cause of AIDS, the initial consolidation of the HIV hypothesis, and the challenges subsequently posed to that hypothesis—has important implications for the study of scientific fact-making in politicized environments. The construction of belief about the causes of AIDS, and the dynamics of controversy, cannot be understood through an analysis of the "scientific field" as traditionally understood
as a self-contained arena in which credentialed researchers are the only important actors. Rather, a highly public and somewhat "open" field has been the site of incessant struggle, negotiation, cooperation, and interaction among a variety of individuals, institutions, and organizations. What are the tactics by which credibility is advanced or attacked in this field? What are the distinctive characteristics of the attempts to resolve controversy in this case?
In an analysis of scientific controversy, Collins and Pinch have suggested that it can be useful to distinguish between struggles waged in what they call the "constitutive forum" and those that are enacted in the "contingent forum." The constitutive forum is the world in which scientific knowledge-production is traditionally believed to unfold—the world of "scientific theorising and experiment and corresponding publication and criticism in the learned journals." The contingent forum, by contrast, includes everything that is supposedly "external" to real science: "popular and semi-popular journals, discussion and gossip, fund raising and publicity seeking, the setting up and joining of professional organisations, the corralling of student followers," and so forth. Collins and Pinch's point is emphatically not that one domain is "scientific" while the other is "extra-scientific." Rather, they seek to show how scientific debates are advanced through recourse to different types of arguments, some of which seek to create the appearance of being "based on universalisable non-contingent premises," while others do not.
Clearly, the AIDS causation controversy has heavily depended on both modes of argumentation. Working within the constitutive forum, AIDS dissenters such as Duesberg have highlighted inconsistencies in the orthodox position, enumerated predictions that have not been fulfilled, pointed to violations of "classical methods" such as Koch's postulates, and made use of medical analogies that compare the conventional wisdom about AIDS to that of other diseases "mistakenly" thought to be caused by microbes. In response, the proponents of the orthodox position have spelled out specific lines of rebuttal, defended the mainstream position through "clarifications" and auxiliary hypotheses, and invoked their own medical analogies that compared AIDS to other conditions where Koch's postulates have not been satisfied. In Susan Leigh Star's terms, both sides have manipulated "hierarchies
of credibility" through "claims that one procedure or approach is more scientifically viable, or technically astute, than another."
At the same time, scientists and medical doctors, not to mention lay participants in the controversy, have been quick to employ the contingent forum to assail the credibility of their opponents. Their mechanisms for doing so have been surprisingly familiar, as revealed by a comparison with the controversy in the 1970s and 1980s over fluoridating public water supplies. In that controversy, as Brian Martin's analysis makes clear, the mainstream position has enjoyed a near-monopoly of scientific credibility, but dissenters have found ways to undercut the credibility of their opponents.
Certainly the most obvious tactic available to the dominant group in such controversies is to try to ignore their opponents—as scientists successfully did with Sonnabend but had more trouble doing with Duesberg. When this tactic fails, the dominant group is typically confronted with the question of whether or not to engage in public debate. Defenders of fluoridation expressed the same sorts of concerns that Fauci and others did about debating Duesberg. One fluoridation enthusiast wrote in the American Journal of Public Health: "A debate simply serves to give more credibility to fluoridation opponents." As Martin has observed, experts who refuse to debate risk being perceived as arrogant, yet simply by engaging in debate they risk undercutting their own expert status by being viewed as partisans. Scientists supporting the dominant position walk a tightrope in trying to retain both their scientific credibility and their moral authority.
In the AIDS causation controversy, as in that over fluoridation, actors on all sides have sought to undermine claims by venting ad hominem attacks against their opponents. In doing so, they have attempted to tarnish their opponents' credibility by challenging either their expert status or their motivations or both. As Martin has noted, supporters of the mainstream position tend to work especially hard to attack the credibility of those opponents who have the most legitimate credentials; and the intensity and range of criticism directed at Duesberg—that he's just a chemist, that he's never worked on human diseases, that it's all a "game" with him and "he has to know he's wrong" —would seem to bear out the general point. Although "more than one can play the game of attacking the credentials, motivations, and honesty of those with opposite views," Martin has said in reference to fluoridation, the majority position tends to win this "battle over reputation in an overwhelming fashion because they have
the preponderance of professional support and especially the backing of professional societies."
In the case of AIDS, defenders of the HIV hypothesis could point not only to all the prominent national and international organizations that agreed that HIV causes AIDS (as Gallo, for example, was apt to do), but could even invoke the general consensus among grassroots activists, who were themselves typically critical of established authority. As ACT UP member Michael Botkin wrote in his column in the Bay Area Reporter , what "bugged" him about the fans of Duesberg was "the way they completely ignore the opinion of the AIDS movement." Noted Botkin: "ACT UP is no dupe of either the federal government or the medical mainstream. Everyone loves a good conspiracy theory, and certainly it's easy to believe that the government is blind, incompetent and corrupt. But if Duesberg's theory has some substance to it, why hasn't it garnered some interest, if not support, in the savvy, skeptical AIDS movement?" This move on Botkin's part might be described as the "monopolization of oppositional credibility."
Some of the most powerful weapons available to the defenders of the dominant position in scientific controversies are the sanctions they can exercise against dissenters. Through control over professional organizations, funding institutions, and journals, they can suppress heretical views and even those who dare voice them. Martin has recorded a variety of examples in the case of fluoridation. When a Minnesota dentist spoke out against fluoridation, his local dental society suspended him for one year without giving him a chance to speak in his own defense. In 1964, when a U.S. sociology student conducted a survey of a group of doctors and discovered that only half the respondents favored fluoridation, the student reportedly was chewed out by an assistant dean "for abusing the good name of her school." An Australian chemistry professor claimed in 1973 that "his staff and equipment had been taken away because of his public opposition to fluoridation." When an article critical of fluoridation was submitted to an Australian journal, it was rejected over the telephone by an editor who claimed "it might encourage the antifluoridationists."
Arguably, these examples are reminiscent of the experiences of Duesberg. The Berkeley scientist has indeed had increasing difficulty getting his views represented in prominent scientific journals, while some of the comments by reviewers and editors have suggested that political considerations (such as protecting the journal's reputation)
have been one factor in the process. He has seen his funding terminated in circumstances that invited suspicion. And he has reported being ostracized by his colleagues and former friends. At the same time, as Martin has pointed out, dissenters in scientific controversies can use such experiences of "unjustifiable" scientific behavior as "a resource in their struggle": "Opponents of fluoridation frequently raise these cases of 'suppression' as showing the political rather than the scientific basis for the promotion of fluoridation."
Criticizing instances of suppression and gatekeeping is one example of a more general tactic that both sides in the causation controversy have employed—what Martin has described as "highligting discrepancies between the stated norms of scientific behavior and the actual behavior of certain scientists." Duesberg has made frequent reference to the charges of fraud that have been brought against Gallo, while opponents of Duesberg have argued that, by speaking to a lay audience, he has sacrificed his scientific integrity. And each side has accused the other of a dogmatism that is antithetical to the true spirit of scientific inquiry: their predictions have been falsified, their arguments have holes in them, yet they refuse to forswear their beliefs. "A powerful hypothesis has to explain and predict," dissenter Harvey Bialy has told Spin: "I ask you, what kind of scientist continues to support a hypothesis that fails to explain and fails to predict?" Writing in the San Francisco Chronicle , Martin Delaney has turned the argument back against Duesberg: "Duesberg is well aware of [contrary] evidence, having been briefed regularly by his faculty peers. Yet he clings to his views, in spite of any and all data, while presenting no original AIDS-related data of his own, a puzzling pattern for someone who claims devotion to science."
Mainstream and Alternative Media
The extensive participation of the media has had important consequences for how credibility struggles have been waged in the AIDS causation controversy. Of course, the media are not monolithic, and different sorts of media have played different kinds of roles. The gay press has been far more receptive to giving space to nonmainstream positions and to citing the noncredentialed as legitimate experts. Alternative news vehicles like Spin , the New York Native , and the Meditel television programs have themselves become important actors in the controversy, intent on advancing certain
positions and demoting others. But as a general rule, the media, by their very presence, have transformed the collective assessment of credibility.
According to Anthony Fauci, "the media are great equalizers in science, which is most disturbing to us scientists"; "any scientist quoted in the media becomes an 'expert.'" Because Duesberg was presented by the media as credible, many people became concerned that the HIV hypothesis is a hoax, Fauci explained, adding that his own sister had called him repeatedly to ask: "Are you sure he's wrong?" Journalistic norms of "balance" impelled reporters to present the controversy as having "two sides"; media consumers, unable to judge for themselves the relative solidity of consensus among AIDS researchers, assumed controversy was rampant.
Martin Delaney, along with other defenders of the established position, has emphasized the penchant for sensationalism and sympathy for anti-establishment views found among at least some journalists and publishers. Yet to dissenters like Duesberg and Jad Adams, the problem is precisely the opposite: the media are the obedient lapdogs of government science. As Duesberg put it: "The press has been functioning like this [taps tape recorder] for the AIDS establishment. They have been Sonys.… Fauci calls the press and there it goes in the New York Times and the Los Angeles Times . Front page. No Fumento balancing it, no second guy writing what you have said. [They] speak directly to the American public. Immediately. That's the difference." Duesberg's critics complain vehemently about the amount of ink that the media have devoted to him, but Duesberg's perspective is completely the reverse: "I mean, measure it against the … 1,000 [articles] on the virus hypothesis that the New York Times alone publishes a year.… You will have a factor of like 1,000 … to one … in their favor. And that's how it works in the propaganda business. That's why Goebbels and others were so successful." In Britain, Duesberg has acknowledged, the media have been more critical, as have been some alternative reporters in the United States like Farber and Lauritsen. But in general the United States "is actually extremely conformist in many ways," Duesberg has complained.
Various analysts have claimed that reporters covering science and medicine—who often fail to have a thorough grasp of the scientific principles at stake—can become especially dependent on their contacts. "Such symbiosis between journalist and source is common in the American media," according to an analysis by Rae Goodell, "but
especially intense in science reporting." One study of U.S. media coverage of the potential swine flue epidemic found that "in spite of the many hundreds of experts who might have been contacted for comment, the same group of medical spokespeople from government authorities was quoted to the virtual exclusion of anyone else." Duesberg has claimed that the same phenomenon is at work in AIDS reporting. Because journalists are so dependent on their official sources, they decline to cover nonmajority views out of fear of being "frozen out": "They won't get further information on the subject from the mainstream.… And then they're out." After all, he has said, "without AIDS, you can't be a science reporter these days."
"My regard for science reporters is very, very low," Duesberg has concluded; and that's one thing that he, Gallo, and Fauci would all seem to agree on. Yet everyone in the AIDS causation controversy also recognizes the singular importance of playing to the media. In explaining why most people accept the orthodox position, Duesberg told California Monthly : "Science is really now a popularity contest, made by newspapers. You hype something in the press, and people take it from there." Duesberg was being critical, but of course, he has played the same game; and he had little choice but to do so if he wanted to advance his claims in the controversy.
Democracy as Rhetoric and Reality
Perhaps the most important factor altering the grounds for credibility in the AIDS causation controversy is the deeply embeded concern with "democracy"—understood in various ways. The most obvious examples of this preoccupation relate to questions of "academic freedom" or "freedom of thought." Duesberg's supporters routinely insisted upon his "right to speak the truth"; a San Francisco Examiner editorial blasting Duesberg nonetheless acknowledged his "right to air his view even in the face of nearly unanimous scientific disapproval." A more profound democratizing claim, also pushed by some of the HIV dissenters, is that the scientific marketplace must be opened up to all those who seek to compete within it. "The 'AIDS establishment' is under the impression that it has a right to govern all discourse on AIDS," complained Celia Farber in Spin . "It feels no one has any business disrupting its conclusions and treatment strategies. But don't all those AIDS posters remind us, 'AIDS is everybody's disease'? Doesn't that include the people who question those who made the posters? Isn't it everyone's debate, too?"
This is a very different kind of claim, one which proposes that science ought to be opened up to anyone who seeks to present knowledge as credible or evaluate the credibility of others. Ironically, even Duesberg has had his doubts about such a project and would reserve science for the scientists. "I'm not excluding anybody else," Duesberg has hastened to add. "It would be great if others would participate too, but they're too easily misled or bought. I mean, [scientists] give them a slide … and it shows something with T-cells … and people say, 'Oh my god, these guys must know everything.' And so you can easily impact a gay activist or counteractivist by this type of information without telling them anything.…" There may indeed be limits to the extent that lay activits can contribute to answering questions such as what causes AIDS. At the same time, there is no avoiding the astonishingly public and contested nature of biomedical science in the late twentieth century, particularly in the AIDS epidemic. Like many of his mainstream critics, Duesberg would have us return to a mythical golden age when researchers did their work in peace, protected from the play of "politics." Yet his own interventions have helped to open the gates to the citadel—and the ordinary people who have gotten the chance to step inside are not likely to surrender that prerogative.
From Causation to Treatment
The democratizing claims of laypeople, while surfacing regularly in the causation controversies, have been even more pronounced in the evolution of debates about treatments for AIDS. These debates, the topic of part two, have been enacted concurrently with the causation controversies, and they involve some of the same protagonists; indeed, references in past chapters to topics such as AZT, which feature prominently in part two, suggest a certain overlap. More profoundly, the intervention of laypeople, particularly within gay communities, in debates about the nature and causation of AIDS from 1981 onward helped construct "knowledge-empowered" communities that could then participate in even more radical ways in debates about treatments.
Yet in certain respects, research into treatment is different from the sort of research involved in determining the cause of AIDS. Since drugs cannot be tested without patients willing to participate in clinical trials, laypeople occupy a central position in the very process of knowledge-making. And since the approval of drugs is often a highly
politicized process involving government agencis, pharmaceutical companies, and other players, debates about the safety and efficacy of treatments travel with particular ease between the pages of scientific publications, the mass media, and—in the case of AIDS—activists publications and the gay and lesbian press. The chapters that follow track the history of research into antiviral AIDS drugs and explore the crucial role of AIDS activists in transforming themselves into experts who could speak credibly about treatments. The interventions of the AIDS movement have had profound implications.for the social construction of belief—for what we come to think is true about the safety and efficacy of antiviral drugs.