Haseltine’s fake slide. Note that the vertical axes have no units, and the chronological notations on the horizontal axis are gibberish.
different measures that could be used. With no satisfactory answer forthcoming, the chairman moved on.
The truth about the Slide Without Units came out in the evening, at a party at the home of Dr. Harris Coulter (author of AIDS and Syphilis: The Hidden Link). In a relaxed and convivial mood, Redfield admitted, in the presence of Duesberg, Rubin, myself, and several other witnesses, that the graph had been prepared to illustrate a theoretical possibility. It had no units on it for the simple reason that it was not based on any data at all. In other words, the slide was a fake.
It is difficult to think of an innocent explanation for Haseltine’s behavior. If he didn’t know what the slide meant, or whether or not it was real, then he shouldn’t have used it. Haseltine presented the slide as though it represented scientific findings, whereas it really represented speculation. It is not unfair to call this kind of misrepresentation, fraud. Nor is it making too much out of one fake slide. If someone will cheat in little things, he will cheat in big things as well. In my book, Haseltine has forfeited his claim to scientific credibility.
Warren Winkelstein, Professor of Biomedical and Environmental Health Sciences, School of Public Health, University of California at Berkeley, gave a talk entitled “Epidemiological Observations on the Causal Nature of the Association Between Infection by the Human Immunodeficiency Virus and the Acquired Immunodeficiency Syndrome”. He was the only panelist to provide printed copies of his talk, something much appreciated by us journalists.
Briefly, the point of Winkelstein’s presentation is that Koch’s postulates should be superseded by new standards for establishing the causal relationship between microbes and disease, and that these standards should be based upon “epidemiology”, or, as it were, correlations of various kinds.
Winkelstein and colleagues in San Francisco, under the auspices of Fauci’s National Institute of Allergy and Infectious Diseases, studied a sample of single men, 25-54 years of age, over a period of three and a half years. Data were collected on HIV antibody status over time, on progression to AIDS, and on various other clinical parameters.
They found that none of the heterosexual males and none of the gay men who remained seronegative developed AIDS, whereas 13% of the men who were seropositive upon entry into the study, and 8% of those who became positive during the course of the study developed AIDS. Further, they found that a progressive decline in T-4 cells occurred among those who were seropositive.
They concluded that epidemiological data from their study, together with data from a related San Francisco study (conducted among a cohort of gay men recruited from VD clinics in 1978 for a hepatitis B study), supported “the hypothesis of a causal association between HIV infection and AIDS.”
All in all, a grim scenario, according to which testing positive for HIV antibodies would truly be a “prognosis for death”. I am skeptical, but as a survey research professional I reserve the right to withhold judgment until I have seen full reports on both San Francisco studies. At minimum such reports would have to include full descriptions of methodology; all questionnaires, recording forms, and field materials; sampling procedures; and computer tabulations.
At any rate, I do not accept the proposition that Koch’s postulates should be abandoned in favor of epidemiological correlations. This would be a step backward, a step away from scientific rigor, a stop towards impressionism and confusion.
Murray Gardner, Chairman of the Department of Pathology, University of California at Davis, spoke about lentiviruses and animals. The man is apparently a failed standup comedian. During his presentation he danced back and forth behind the table, gesturing wildly, urging the audience to laugh along with him at the absurdity of doubting, even for a moment, that HIV was the cause of AIDS. We were told that the animals had “little understanding of co-factors”, that their diseases had “nothing to do with lifestyle”, and so on. Gardner had begun his clown act even earlier, making faces during Rubin’s presentation.
Virtually nothing Gardner said was relevant, and little was memorable, except perhaps a few mistakes. A slide of his referred to the “pathogenicity of new HIV strains, e.g., HIV-2”. This is wrong: HIV-1 and HIV-2 are not different strains of each other; they are completely different viruses; they differ in genetic structure by up to 60%; they do not have a closely-related common ancestor.
On this basis Dr. Joseph Sonnabend in New York City has formulated an “evolutionary argument” against the HIV hypothesis, which runs roughly as follows: There is no longer just one “AIDS virus”; there are several, perhaps as many as four or five at last count. It is now claimed that both HIV-1 and HIV-2 are capable of causing AIDS, a disease which allegedly appeared in the world for the first time only a few years ago. However, viruses are products of evolution, and very ancient — there is no such thing as a “new” virus. The proposition that, within the space of a few years, two different viruses, each capable of causing the same new disease, should have come into being, or should have gone from an animal reservoir to susceptible human populations, is beyond the bounds of probability.
Gardner concluded his presentation by winking at the audience. It reminded me of one critic’s comment on a cheaply made horror movie, that the zombies were less frightening than the attempts at humor.
Roger Detels, Professor of Public Health, University of California at Los Angeles, began his talk by saying that it was good to continue questioning judgments. In context, this amounted to an apology to Duesberg and Rubin for the rudeness with which they had been treated. It was a gracious gesture on his part.
Detels discussed the San Francisco “Multi-Center AIDS Cohort Study”, in which an annual “attack rate” of 5% was found among the seropositive gay men studied. That is, each year 5% of the seropositives came down with AIDS. (Harry Rubin was to point out later, that if 1-3 million Americans are seropositive, according to CDC estimates, and if the annual attack rate is 5%, simple arithmetic indicates that every year 50,000 to 150,000 people ought to develop AIDS.)
During the question period, pathogenesis was mentioned again, and Haseltine entered the fray, insisting that there were plenty of mechanisms that could explain pathogenesis, and that it was not necessary to discuss it.
Questions From The Audience
The first audience participant was Harvey Bialy, Research Editor of Bio/Technology. His remarks can be found in more detail in an editorial in the February issue of Bio/Technology 6. The gist is that several recent articles have cited antigenemia findings to suggest that HIV may, after all, be active during the fatal, late stages of AIDS. However, the papers contain serious mathematical and other discrepancies. Bialy maintained that it was the responsibility of scientists, as well as journalists, to look at data critically and ask the hard questions.
The second speaker from the audience was Dr. Harris Coulter, who asked whether findings from the San Francisco City Clinic study, based on a sample of gay men who had hepatitis B, and who were highly promiscuous and heavily into recreational drugs, could be extrapolated to all of the people in the U.S. who were seropositive. The epidemiologists were either unable or unwilling to answer his question. Coulter persisted, asking the question in several different ways, each of which was perfectly clear. But the “AIDS experts” could not respond. This was truly amazing, for the question was one of the most basic in all of statistics: How representative is a sample of a particular universe? Can one project findings from the sample to the target universe?
Next Dr. Nathaniel Lehrman spoke, emphasizing the need to re-examine the etiology of AIDS, not only because of the questions raised by Duesberg and others, but because its epidemiology is far more consistent with a toxic illness than with an infectious one. How could AIDS be only an infection, and spreading so rapidly, when, according to Surgeon General C. Everett Koop, M.D., not one of 750 accidental inoculees with the blood or body fluids of known AIDS patients developed the disease, and only three then developed antibodies to HIV?
Chemical causes of immune deficiency, stated Lehrman, have long been known, and one group of chemicals, known to produce immune suppression, may be a cause of AIDS in the homosexual community: inhaled nitrites, or “poppers”. Could other chemicals also be involved in producing immune suppression and AIDS? Lehrman concluded by saying that the possibility that chemical toxicity plays a significant causal role in AIDS ought to be investigated, and that additional methods in diagnosing, treating and researching the syndrome should be adopted. One such step would be spectrophotometric and similar investigation of AIDS patients for unusual, immune-suppressive substances within their bodies.
I spoke next, and said it was high time that those who advanced the hypothesis that HIV was the cause of AIDS should publish a monograph in an appropriate journal, which would bring together all the evidence supporting their hypothesis, which would take into account the critiques made by Duesberg and others, and which would contain proper references for all assertions made. Then I said that the epidemiological research on AIDS had been very poor, completely unacceptable by the standards of professional survey research. Ever since 1984, Public Health Service surveys have concentrated only on such things as “modes of transmission”, or “risk factors for seroconversion”, as a result of which we know almost nothing about the characteristics of PWAs. We have no idea what the IV drug users with AIDS are like, other than the “risk group” label that has been slapped on them. Finally, I said it was disgraceful that AZT was still being marketed, a poisonous drug without a single scientifically-established benefit. When would the AIDS establishment admit that the AZT trials, on which approval of the drug was based, were fraudulent? 7
Finally, Michael Specter, a reporter from the Washington Post, demanded that Duesberg give him a yes or no answer to the question, “Do you still maintain that someone should be overjoyed to find out he is positive?” When Duesberg paused, the way one does when confronted with an obstreperous barbarian, Specter started yelling, “Answer the question! Yes or No? Why won’t you answer the question?” Duesberg, when he got a chance, replied that he would answer the question, but in his own words, not Specter’s. The nuances of his answer were not appreciated.
For the debate on the cause(s) of AIDS to move forward, a number of questions of fact must be resolved, with proper references given for all assertions: Does HIV kill cells in vivo? If so, how? Is HIV really “more complex in its genetic makeup than any other known retrovirus” (as asserted in AmFAR’s “Review of Operations: 1985-1986”)? From what percentage of PWAs can HIV be isolated? From what percentage of PWAs can pro-viral DNA be detected? What is the definition of a “good lab”? Is viremia found in PWAs? If so, what virus titers are obtained, when, how, etc.? Are there (as asserted by Gallo et al.) both pathogenic and non-pathogenic strains of HIV? If so, how do they differ? Can “nude mice” really mount a vigorous immune response (as asserted by Haseltine)? Is a full report available on the epidemiological research conducted in San Francisco?
The forum exposed the bankruptcy of the arguments used by the HIV advocates. Only a few weeks ago they were trotting out at least half a dozen speculative mechanisms to explain how HIV might cause AIDS; during the forum, such speculations were abandoned, and the official line was, “We don’t need to explain pathogenesis.” The “AIDS virus” crowd cannot agree on even the most crucial questions of fact, as indicated above. At one moment HIV is ferociously killing T-cells; the next moment, “AIDS experts” are desperately scrounging around for “indirect mechanisms”. “Epidemiology” has been called in as a last ditch effort to rescue the HIV hypothesis, and yet the epidemiology conducted by the AIDS establishment to date has been quite bad, totally unacceptable by the standards of professional survey research (of which “epidemiology” is a subspecies). While the San Francisco studies may “strongly support” the HIV hypothesis, they could not prove it, even if the data were correct (and this cannot be determined until a proper report is issued), because there remain alternative explanations to account for the correlation between HIV antibodies and AIDS — namely, that HIV is itself an opportunistic infection in the AID Syndrome, that HIV is a marker for AIDS.
I am more convinced than ever that HIV is not the cause of AIDS. If the HIV advocates were sure of their hypothesis, they would want to enlighten Duesberg and the rest of us; they would want to publish their arguments in a proper scientific journal, complete with references. They would not need to resort to stonewalling, deception, and personal abuse.