(Rethinking AIDS: The Tragic Cost of Premature Consensus, by Robert S. Root-Bernstein, Free Press, 512 pp. $27.95.)
Root-Bernstein is joined in his heresy most notably by the biologist Pete Duesberg at Berkeley, whose views have been publicized in journals ranging from Policy Review to the Atlantic.
Although there are apparent divergences between them, both Duesberg and Root-Bernstein argue that for the last eight year we have been going down the wrong path by treating the Human Immunodeficiency Virus (HIV) as necessary to cause AIDS.
Duesberg claims that HIV does not cause AIDS and does not contribute to it in any way, shape, or form; rather, HIV is a harmless "hitchhiker" which somehow manages to find its way into the bodies of persons with immuno-compromised systems. Root-Bernstein is not so quick to dismiss any role for HIV. He grants that there appears to be a strong if incomplete overlap between persons infected with HIV and those who eventually contract and die of AIDS. But his thesis, in a nutshell, is that "HIV is neither necessary nor sufficient to cause AIDS."
Root-Bernstein espouses what has been called the "multiple-hit" theory according to which repeated blows from such sources as recreational drugs, sexually transmitted diseases, and the antibiotics used to treat those diseases damage the immune system so severely as to allow the opportunistic infections associated with AIDS to strike and kill.
"Every person with AIDS for whom there is sufficient documentation," he writes, "has some subset of . . . risk factors" associated with immune suppressants. By failing to look for these co-factors, says Root-Bernstein, scientists have been terribly, terribly remiss. For if we can eliminate those factors, we can essentially eliminate AIDS.
Why is HIV not sufficient to cause AIDS? Taking a tack from Duesberg, Root-Bernstein attributes tremendous scientific importance to the fact that the HIV-AIDS connection does not satisfy Kochs postulates, a system devised a century ago by Robert Koch, a German physician, to establish the relationhip between a disease and its suspected cause. But Koch, though a brilliant researcher, was not the epidemiological equivalent of Moses the Lawgiver, and, in any event, viruses had not even been discovered when he formulated his rules.
It is certainly true that the HIV-AIDS link does not satisfy all four of Kochs postulates. In particular "there is no doubt," as Root-Bernstein writes, that it does not satisfy the third postulate: namely, that the microbe in question must be able to induce disease in healthy test animals. But this is only because we are ethically forbidden to use humans as test animals when fatal diseases are involved. Three years ago, I challenged Duesberg to make himself a test animal by injecting himself with purified HIV. He declined.
Root-Bernstein makes much of the fact that HIV does not induce AIDS in chimpanzees and other nonhumans, but we know of a number of pathogens which, being species-specific, are exceptions in this way. The myxomatosis virus, artificially introduced into Australia to control the feral rabbit population, succeeded in killing millions of the animals but no humans. Feline leukemia virus kills huge numbers of cats but their owners are not afflicted. Researchers despaired of finding a test animal to develop treatments for Hansens disease (leprosy) until someone discovered the disease in armadillos. How can Root-Bernstein not know all this?
To establish the other half of his thesis, that HIV is not necessary to cause AIDS, Root-Bernstein claims that persons who develop AIDS "virtually without exception are unhealthy, immuno-compromised people even before they contract HIV and long before they develop AIDS." But the truth of this assertion rests on a hopelessly expansive definition of "unhealthy" and "immuno-compromised."
Root-Bernstein spends an entire chapter going down his list of immune suppressants, which include everything from semen to addictive and "recreational" drugs to anesthesia and surgery to prescription drugs to malnutrition to blood transfusions to old age. By the time he is through, practically all of us could be said to be suffering from some sort of immune dysfunction.
There are, however, many levels among the factors that compromise the immune svstem. Some are so tiny as to show up only in laboratory tests. Others may cause one to be more susceptible to colds, or make a cold last longer than it otherwise would. Only the most severe will expose one to the sorts of life threatening illnesses that kill AIDS victims, Yet Root-Bernstein essentially treats all of these as severe immune suppressants.
Thus he cites numerous studies of HIV-negative homosexual men who have "significant reduction in T-4" white blood cells (part of the bodys immune system) or "significantly reduced T-cell and B-cell activity." But he neglects to explain what this means, namely, that the reductions were measurable in a laboratory test, not that they necessarily had developed to the point where opportunistic diseases could take hold.
Last year, a friend and I took an unauthorized detour off a Pacific Coast Highway cliff, and she sustained injuries that led to a virtual field day of immune suppression. The contributing factors included shock, brain surgery, anesthesia, the anti-ulcerative medicine Tagamet, antibiotics, a urinary tract infection from a catheter, multiple blood transfusions, and sudden weight loss. What she did not get was AIDS, or anything resembling it.
Indeed, how could she? Only the most profound immune dysfunction, such as infection with HIV or treatment with a powerful immune-suppressing drug used in transplant operations to prevent organ rejection, opens one up to a disease like PCP pneumonia (which shows up about a third of the time as one of the diseases that lead to a diagnosis of AIDS). Very few PCP cases have ever been recorded in individuals who fall outside these narrowly defined conditions.
Recently a team of researchers decided to test the hypothesis, as stated by Peter Duesberg, that "either drug consumption (frequently associated with malnutrition) by recently established behavioral groups or conventional clinical deficiencies are necessary and sufficient to cause indicator diseases of AIDS." They compared a set of heterosexuals who were heavy drug users but negative for HIV with homosexuals who were heavy drug users and were either positive or negative for the virus.
Writing about their results in the March 11, 1993 issue of Nature (a date that coincided almost exactly with the publication of Rethinking AIDS), the researchers reported that among the homosexuals who were HIV-positive at the beginning of the study, over half had contracted AIDS and most had died. Among the homosexuals who were negative in the beginning and stayed negative, about 2 percent had died but none had been diagnosed with AIDS even when HIV status was excluded as part of the AIDS definition. Among the HIV-negative heterosexuals, less than 1 percent had died and none had gotten AIDS.
In addition to devastating the drug-use-causes-AIDS thesis, this study shows as close a correlation between pathogen and disease as one could ever hope to attain — Koch and his postulates notwithstanding.
According to Duesberg, what killed Bergalis was the anti-viral drug AZT; but this is nonsense, because she began taking AZT only after her immune system had started to plummet. According to Root-Bernstein, on the other hand, she could have lied about using drugs or about other factors.
He may or may not be right about this, but are we now to take the mere possibility that someone is lying as grounds for an at-risk classification? And what about the wives of HIV-infected hemophiliacs and blood-transfusion victims who have been getting HIV and then AIDS? Root-Bernstein would say that they must have done something independently to suppress their own immune systems, but surely there is another, more obvious explanation, namely, sexual intercourse.
Root-Bernstein claims that there have been cases of "AIDS without HIV" and cites what amount to perhaps a few dozen. The disclosure of some of these cases caused quite a stir at the international AIDS conference held last year in Amsterdam. But all diseases share symptoms with other diseases — the more so AIDS, which by definition is a syndrome entailing the manifestation of other diseases.
Just as persons who appear to have textbook cases of tuberculosis can test negative for the microbe that causes the disease, persons who look very much as if they have AIDS can fail to test positive for the AIDS virus. But these few dozen cases of "AIDS-without-HIV" must be placed alongside the hundreds of thousands of Americans who appear to have AIDS and who do test HIV-positive.
To be sure, there may be co-factors that increase the rate at which HIV decimates the immune system; blocking these co-factors might greatly increase the length and quality of life for affected persons. Despite what Root-Bernstein would have us think, though, scientists have been devoting a great deal of research to finding them. Everything from genetic factors to mental attitude to exposure to sunlight has been explored.
One recent study links smoking to a doubling of the speed at which infection progresses to full-blown AIDS, but in general the efforts to identify co-factors have not had much success.
Toward the end of Rethinking AIDS, Root-Bernstein informs us that even "John Maddox, editor of the eminent journal Nature, has written that he should have given critics of the HIV theory, such as Peter Duesberg, room to express their concerns." But in light of the drug-user study I mentioned above, and two more recent articles in Nature on the activity of HIV within the body, Maddox has since editorialized that "Duesberg, having led many people with AIDS on a speculative path, should now admit the likelihood that he is mistaken."
In short, the AIDS heretics have been given "room to express their concerns," and have been found wanting.
Read Michael Fumentos additional work on AIDS.