What Causes AIDS?

The debate continues

From the December 1994 issue

(Page 7 of 7)

The absence of an animal model is not cured by tall tales about the so-called simian immunodeficiency virus. SIV does not cause a syndrome like AIDS in animals. The distinctive and improbable claim of the HIV/AIDS hypothesis is that the HIV supposedly damages the immune system only after the immune system has successfully countered the primary infection and reduced viral activity to negligible levels. "SIV disease" follows the primary infection closely, and does not occur after a latency period of ten years during which viral activity in the blood is practically non-existent. It also occurs only in laboratory animals, who tend to have weakened immune systems already. The same retrovirus is found in wild populations causing no ill effects. Other claims of "lentiviruses" causing diseases in animals many years after infection are also controverted in the scientific literature, and may reflect the enthusiasm of virus hunters to attribute disease conditions to the viruses they have discovered.

Because of the absence of an animal model, or plausible mechanism for T-cell destruction by an inactive virus, the whole case for HIV causation rests on correlation. But very sick persons with damaged immune systems carry many microbes, and it is impossible with correlation studies alone to prove that a particular microbe is the effective cause of the syndrome rather than a mere "passenger." To distinguish cause from effect, studies must be carefully controlled. Above all, the syndrome must be defined in a way that does not prejudice the outcome. But the CDC's response to our article admits that AIDS is defined as a range of disease conditions accompanied by real or suspected HIV infection, so that HIV causation is presumed in the definition of the syndrome. The CDC's response, translated from the bureaucratese, is simply "that is how we do it around here." Use of a biased definition that assumes the very correlation to be proved is professional malfeasance on its face.

Things are even worse than that. Tens of thousands of cases of persons with diseases like KS (this is the "small percentage" to which the CDC refers) have been diagnosed on presumptive criteria without antibody tests, and this practice is still allowed. Duesberg's estimate of several thousand American cases of AIDS without HIV comes from examples in the medical literature where individuals were diagnosed with AIDS on the basis of disease conditions or immune deficiencies and then the diagnosis was reversed when HIV was not found. We consider this estimate conservative, because in logic every person with a condition that would be diagnosed as AIDS if an antibody test were positive (like tuberculosis, for example) is a case of AIDS without HIV. The CDC acknowledges only 100 or so cases because it employs a much narrower definition of "AIDS" when HIV is not present than when it is, and it then dismisses the remaining cases because they "differ epidemiologically" from AIDS-meaning apparently that they are not linked to HIV! That the CDC does not understand the need to define the syndrome independently of the hypothesized cause is further evidence that their experts never did the epidemiological work impartially in the first place.

That brings us to the San Francisco study defended by Warren Winkelstein, which supports a correlation between AIDS-defining diseases and HIV, but not drugs, in a population of San Francisco men. Tom Bethell's letter points out that this study was vigorously criticized at the AAAS meeting in San Francisco in June. We are prepared to pursue this criticism in an appropriate scientific forum. For present purposes, readers need to understand primarily that Winkelstein and Michael Fumento are misrepresenting the scientific method. Epidemiology (i.e., correlation) is a useful tool for identifying a possible causative agent, and especially for rejecting impossible ones, but to prove cause on this basis alone is unwarranted. Fumento's example of yellow fever is instructive. Walter Reed's mosquito hypothesis was confirmed by his success in eliminating the disease. HIV causation could be confirmed by similar success, or by a demonstration of the mechanism of causation, or by meeting Koch's postulates, the traditional rules for confirming a causation hypothesis. If the mosquito hypothesis had produced no results after 10 years of trying, Walter Reed would no doubt have been wise enough to consider other possibilities.

There are three reasons for using correlation as an indicator rather than as sufficient proof of causation in itself. First, even if the putative cause (HIV) is highly correlated with the syndrome (one or more of 30 AIDS-defining diseases), correlation studies cannot tell us whether or not the true cause is a third factor or combination of factors which is correlated with HIV. Gay men in San Francisco who are HIV positive, for example, are also likely to have a lot else in common. The correlation would be much more convincing if it were equally strong in all populations, which is why we recommend strictly controlled studies in all the risk groups, and especially in Africa.

Second, it is naive to present HIV correlation studies as if they were naked data lying around for some unbiased scientist to interpret. The HIV hypothesis was fixed in concrete as "scientific fact" by Dr. Gallo's 1984 press conference, and the studies that followed, including the Winkelstein and Schechter studies, were performed by researchers who never questioned the ruling paradigm and would have lost their grants if they had. A multi- billion-dollar research industry will always be able to produce studies by true believers that support its position; the amazing thing is that the HIV industry has to rely so heavily upon two studies of North American men's groups.

To bring up the reality of bias is not to question the integrity of any individual scientist. It is merely to point out that the reason "double blind" studies are essential in medicine is that even the best doctors tend to see what they expect to see-and systematically fail to see what they do not want to see. When we learn that the NIH and CDC's epidemiologists saw nothing wrong with using a biased definition of AIDS (diseases plus real or suspected HIV) in conducting the studies that supposedly established the correlation, we are on notice to be skeptical of everything they say.

Third, AIDS as officially defined is a complex syndrome defined differently on different continents, and manifesting different disease symptoms in different risk groups. The point is not merely whether HIV causes something, or even something serious. It does seem to cause flu symptoms in some persons during the initial infection, when it is multiplying freely in the blood stream and is easy to find. A positive reaction on antibody tests does seem highly correlated in certain populations of gay men with some of the diseases grouped together as "AIDS." This kind of information may have been sufficient to identify HIV as a suspect, but it is not sufficient to justify disregarding everything else we have learned that puts the HIV theory in doubt. HIV clearly is not the sole or primary cause of KS, despite the status of KS as one of the most important AIDS-defining diseases. There is ample reason to question whether HIV infection causes a spectrum of 30 or so diseases many years later by a mechanism that no one can determine when it often can hardly be found at all. It is highly unlikely that the same virus causes some diseases mainly in men in North America, and different diseases in men and women equally elsewhere. An epidemiological study of a group of San Francisco (or Vancouver) men is inherently incapable of validating a theory that encompasses so many contradictions and anomalies.

We do not necessarily dispute Winkelstein's conclusion that, at least in certain populations, "Regardless of whether or not HIV infection causes AIDS, it is a strong predictor of premature death." Persons who are sick from a lot of different things tend to have a lot of different things in their bloodstream, and some of these cause positive reactions on HIV antibody tests. Our skepticism about the HIV hypothesis should not encourage anyone to engage in risky behavior. We mainly agree with the HIV doctors about prudent health rules, except insofar as they would tell people that they may use poppers and similar recreational drugs without fear of damage to their immune systems.

We would merely add that prudent people should especially avoid poisons like AZT and related drugs, which destroy immune system cells and other cells and provide no demonstrable benefit. They should rise up in outrage against dogmatists who want to administer AZT to pregnant women and infants when no adequately controlled studies have been performed to justify this reckless medical practice. They should start questioning loosely supported claims about the spread of HIV in Asia and Africa, and they should demand that impartial, controlled studies be performed to determine what is really going on.

Fumento to the contrary notwithstanding, we do not urge anyone to "forget" any studies or to ignore any evidence. Our point is that the rethinking of HIV science that the top NIH officials admit is necessary is meaningless unless they also reconsider the basic diagnosis. Our research program is simple: Perform the unbiased, carefully controlled epidemiological studies in all risk groups that should have been done in the first place. Employ an unbiased definition of AIDS. Don't assume the HIV hypothesis and defend it with ad hoc arguments and fudge factors; test its various claims impartially. Why is this scientific common sense resisted so bitterly?

It was not unreasonable for the molecular biologists and the epidemiologists to consider HIV a suspect back in 1984. They all assumed that Dr. Gallo had caught HIV in the act of destroying the immune system, and a high percentage of the cases under study did have something in their blood that reacted positively to the antibody tests. But a lot has changed since 1984.

It turns out that HIV isn't really doing anything observable to the immune system, that predictions based on the HIV theory are continually being falsified, that the HIV stalwarts rely more and more on the least reliable statistics, that the antibody tests aren't reliable indicators of HIV activity in the bloodstream, and that even researchers dedicated to proving a perfect correlation between HIV and AIDS have to admit to a lot of nonconforming examples.

Ten years after 1984, the question is whether a biomedical research establishment that jumped prematurely to a conclusion wants to re-examine that conclusion by proper scientific methods and learn the truth, or whether it would prefer to keep its mistakes hidden as long as possible.

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