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."