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.