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."