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.^[27] Why these types of studies? Implicitly or explicitly, researchers had Koch's postulates—or similar criteria—in the backs of their minds.^[28] 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 Describing the "unpublished observations" of ten seropositive blood donors whose recipients later developed AIDS, Wong-Staal and Gallo commented that "nature has indirectly fulfilled one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."^[29]

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.^[30]

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";^[31] but technically no chimp had developed AIDS (and for a decade, no chimp would).^[32] 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.^[33]

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.^[34] 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."^[35] 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.^[36] 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^[37] 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.