WHAT CAUSES AIDS?
The Debate Continues
Reason, Dec. 1994
In the June issue of REASON, Charles A. Thomas Jr., Kary B. Mullis, and
Phillip E. Johnson argued that the hypothesis that HIV causes argued that the
hypothesis that HIV causes AIDS has been falsified and that it is important to
reopen scientific debate on the question. REASON takes no stand on the former
conclusion-though the editors believe the article made a strong case-but it
strongly supports the latter.
To further that debate, REASON solicited letters from scientists pursuing AIDS
research and others with a strong interest in the subject, some of whom
responded. We also received numerous letters from readers. A selection is
printed here, along with the authors' reply.
"What Causes AIDS? It's An Open Question" provided a lucid explanation for
skepticism over the role of HIV in AIDS. As an African historian, I am appalled by
the unscientific diagnoses of AIDS in Africa and the persistence of Western racist
myths about sexual promiscuity on that continent. "What Causes AIDS?" gives my
students a valuable introductory source to begin rethinking AIDS in Africa.
As chairman of the History and Philosophy of Science Section for the Pacific
Division of the American Association for the Advancement of Science (AAAS), I
included Thomas, Mullis, and Johnson at a symposium on "The Role of HIV in
AIDS: Why There is Still a Controversy," which I organized for our June 1994
conference in San Francisco. Even though the symposium was approved by the
executive committee of the Pacific Division in January and publicized in division
newsletters sent to 30,000 members, the AIDS establishment mounted a
behind-the-scenes effort in May to either cancel the symposium or seriously
The increased desperation of the HIV=AIDS orthodoxy among journalists and
within the biomedical research establishment will prompt more attempts to stifle
debate. Their efforts to mislead the public through scientific censorship are doomed
to failure as long as we can count on courageous publications like Reason.
Charles L. Geshekter
Professor of History
California State University, Chico
I was glad to see Reason entering the HIV/AIDS fray. My own experience in
writing about this subject has convinced me that Thomas, Mullis, and Johnson are
Often cited as evidence that HIV, and not drug use, is the real cause of AIDS, is a
paper published in Nature, written by Ascher, Sheppard, and Winkelstein. I was
surprised to read, in a March 11, 1993, story by Gina Kolata in The New York
Times that this Nature article had been written specifically in response to an op-ed
piece I had written for the San Francisco Chronicle six months earlier. "Dr. Ascher
and his colleagues wrote their paper in response to a challenge by Tom Bethell,"
Kolata wrote, quoting Ascher as saying that "Tom Bethell threw down the
gauntlet," forcing them to do the study. I can only say that this must be the first
medical study ever written specifically in response to an op-ed piece by a journalist,
and then published by Nature. Any doubts that I may have had about the political
character of AIDS vanished when I read Kolata's weird article. The fact is, I am
now convinced, AIDS is not a disease at all-it is a government program.
At the June AAAS meeting in San Francisco. Bryan Ellison, a graduate student in
Molecular and Cell Biology at U.C. Berkeley, presented a reappraisal of the Ascher
study, having obtained the raw data on which it was based. Ascher et al. had
examined a cohort of about 1, 000 men in San Francisco and had found that,
surprise, surprise, all of those who developed AIDS were HIV positive! Once
again, however, the definition of AIDS included HIV positivity. The real question
was: How many AIDS-defining diseases were to be found in the HIV-negative
cohort? Ascher et al. had failed to report this key information. But the raw data
from the original survey showed at least 45, and possibly as many as 200,
AIDS-related diseases among the HIV-negative men, Ellison told the AAAS
"What Causes AIDS?" exaggerated some facts out of context to reach outrageous
and misleading conclusions.
HIV is a silent, fatal, contagious disease that is in fact spreading now into the
heterosexual population, especially adolescents, and the usual public-health
strategies that have been employed for decades to halt the spread of the virus have
not been applied to this illness due to certain political lobbies. These same groups
love to utilize "AIDS" data rather than HIV prevalence since, with a silent 10-year
latency, AIDS data tells you what was happening 10 years ago.
Recently, the Centers for Disease Control released data from 22 of the 24 states
reporting HIV cases (not including California, New York, etc. where rates are
highest). For male teenagers, the ratio of HIV to AIDS cases is eight to one. For
female teenagers,the ratio is 22 to 1. When you analyze AIDS data, you don't see
the epidemic coming because you're looking backward, the wrong direction. For
Thomas et al. to claim that the virus "remains almost entirely confined to the
original risk groups" is untrue and dangerously lackadaisical. Summarizing the
recently released CDC data, AIDS Alert, October 1993, concludes, "the fastest
growing mode of infection is through heterosexual contact while intravenous drug
use has leveled and homosexual transmission has declined."
Thomas et al. present "evidence" that HIV does not lead to AIDS because many
people have HIV without these diseases. This is entirely consistent with the long
latency period. And the vast majority of those dying of AIDS have HIV.
The authors wrongly contend that the HIV antibody test is plagued by false
positives. The test is extremely sensitive, and final reporting is made specific by the
confirmatory Western Blot and other back-up tests. Col. Donald Burke, a research
virologist at Walter Reed Hospital, has personally supervised several million HIV
blood tests for the routine Army testing of recruits. His statistics demonstrated that
HIV testing resulted in less than one false-positive in one million blood tests.
It is frustrating for me to see Thomas et al. use the fascinating mysteries of this
disease to bring fuel to the fire of those who have been hindering a prudent
scientific approach to this epidemic.
Daniel Cosgrove, M.D.
Palm Springs, CA
As a scientist, albeit not an expert on AIDS, I would like to explain why I did not
find the article by Thomas, Mullis, and Johnson to be very convincing. First, it is
no surprise that some people who are HIV-negative fall ill with the diseases
associated with AIDS (Kaposi' s Sarcoma, certain types of pneumonia, etc.). These
diseases are not new. Factors other than HIV virus can damage the immune system
and may make individuals susceptible to these, and other, illnesses.
What we have been seeing since the early 1980s is a much larger number of
immunodeficient individuals exhibiting a number of hitherto uncommon illnesses,
who are also infected with the HIV virus. We also see that a significant number of
people lacking the symptoms of AIDS soon develop them after being exposed to
the bodily fluids of individuals infected with HIV.
In the absence of any other explanation, simple induction leads us to the conclusion
that HIV is either the cause, or part of the cause, of AIDS. True, in the absence of
a causal mechanism for AIDS this is not final proof that HIV causes AIDS, but
currently it is the best explanation we have.
Second, it is also not surprising that some HIV-positive individuals do not develop
the symptoms of AIDS. In the population of millions of HIV-infected individuals, it
is to be expected that genetic diversity should ensure that at least some individuals
are resistant or even immune to HIV. If this were not so, the plethora of other
diseases and plagues that humans were subject to before the discovery of vaccines,
antibiotics, and modern medicine would have long since caused our species to
become extinct. In this respect, HIV infection should be no different.
If the authors and their intellectual ally, Dr. Peter Duesberg, are convinced that
HIV does not cause AIDS, then let them put forth an alternative hypothesis and
purpose a course of research to determine the true cause of AIDS. Creative
research is much more difficult than criticizing the efforts of others.
Ron M. Kagan
Ph.D. Candidate, Biochemistry
University of California
Los Angeles, CA
Is HIV "a conventional retrovirus with a very simple genetic organization" ? Well,
most retroviruses can get by with three or four genes, whereas HIV has nine. All
other viruses in the subfamily to which HIV belongs (the lentiviruses) are
responsible for fatal immune-cell disease in animals (sheep, cattle, horses, cats,
monkeys), and scientists have not been able to develop a cure for any of these
Was the HIV=AIDS dogma established, without scientific foundation, by a press
conference? No. Although considerable publicity was attached to a premature
announcement by Dr. Gallo in 1984, there was agreement by consensus, not by
fiat. The relevant scientific papers were published a few days later in the May 4
issue of the journal Science and served as confirmatory evidence of the strong
association between AIDS and a retrovirus similar to one that had been discovered
the year before in a wide variety of AIDS patients by researchers at the Pasteur
Institute in France.
Several other investigators in this same time period were also in the process of
isolating a virus from their AIDS patients (Karpas in England, Rossi in Italy,
Francis in Atlanta, and Levy in San Francisco). All of these viruses, initially called
by different names, eventually turned out to be variants of the same virus. The
name was not standardized to HIV until 1986.
Is there not "even a theoretical explanation for the disease-causing mechanism"? Of
course there is. Although the immune response to the initial HIV infection soon
eliminates free virus particles froth the bloodstream, it is usually unable to eliminate
the virus if it has already infected cells in the organs of the lymphatic system. Once
there, the virus slowly propagates from cell to cell like a cancer, gradually
infiltrating these organs (the lymph nodes, spleen, thymus, tonsils, adenoids,
appendix, etc.), many of which are redundant and can withstand a lot of damage
before there are any obvious symptoms of impaired function. Blood cells that are
susceptible to the virus, called T-helper lymphocytes, continually circulate through
the diseased lymphatic organs and are gradually trapped and killed off. The part
that is not understood, and for which "increasingly exotic causal mechanisms" have
been proposed, is whether the virus kills them directly, or the immune system itself
kills them because the mere presence of the virus has made them abnormal.
Are HIV-negative cases of AIDS being ignored or covered up by the medical
establishment? Hardly. In 1986, a patient from West Africa with obvious AIDS
was found to be negative for HIV. This led to the discovery of a defined
AIDS-causing lentivirus now called HIV-2.
Are the opportunistic infections that are characteristic of AIDS sometimes found in
the absence of HIV? Of course. They are simply rare in the general population, not
non-existent! They were discovered and named long before AIDS came along, and
can get the upper hand in anyone whose immune system is temporarily depressed.
Thousands of such people "disappear from the official statistics" because they get
well, not because the CDC is engaged in some sort of nefarious cover-up.
Nevertheless, since HIV is now so widely used as a diagnostic test for AIDS, the
possibility does exist that an epidemic of HIV-negative AIDS could occur without
our realizing it from standard statistics. This is why an exhaustive search for
HIV-negative patients with profound unexplained immunodeficiency was
undertaken in 1992. Less than 100 scattered cases were identified worldwide. They
were studied and their disease given a new name (ICL) because their immune
abnormalities were found to differ slightly from those typical of AIDS. In any case,
the number of such patients compared to the hundreds of thousands of AIDS
patients reported around the world is vanishingly small.
If the authors of this article truly believe that there is an epidemic of deaths from
sustained immune deficiency that can not be explained by HIV or other known
causes, I urge them to avoid the entrenched HIV=AIDS hypothesis by reporting
these cases to the CDC as a new disease, rather than attempting to link them to
Thomas, Mullis, and Johnson state that "chimps have repeatedly been infected with
HIV, but none of them have developed HIV." True enough, and none ever will.
Chimps are not susceptible to HIV because that virus targets the human, not
simian, genome. But chimps infected with the SIV (simian immunodeficiency virus,
a virus genetically similar but not identical to HIV) do develop suppressed immune
systems and the symptoms of AIDS. It is inexplicable that these writers do not
recognize that a chimp's failure to contract AIDS from HIV no more addresses the
consequences of HIV infection in humans than does the human failure to contract
feline leukemia virus indicate that cats cannot contract leukemia either, This
impressive display of epidemiological ignorance casts doubt on their ability to
interpret evidence wisely, but there's more.
They say the virus is generally not detectable in people with advanced AIDS; a
large body of literature exists confirming that the virus is present and detectable
during all stages of the disease. They claim HIV is a simple retrovirus that is not
capable of the sophisticated behavior it apparently displays; epidemiologists have
described HIV as a complex virus whose full genome is not yet understood.
Thomas, Mullis, and Johnson imply that Warner C. Green in an article in the
September 1993 Scientific American acknowledges the supposed tenuous
connection between HIV and AIDS. Green does nothing of the sort. In fact, in that
article he writes: "I must emphasize that all responsible opinion holds that HIV is
indeed the cause of AIDS. A small number of cases of people with immune
deficiency who are not infected with HIV received inappropriately widespread
publicity last year, which fostered the unsubstantiated notion that there is another
cause of AIDS not detected by current blood tests."
The authors also suggest that causality between HIV and AIDS has not been
proven; all we have, they say, is a correlation between the two. Science, however,
will never be able to "prove" that HIV causes AIDS any more that it can prove that
varicella causes chicken pox. Proving a positive is an impossibility (an assertion can
only be disproven). All relationships between vital infections and resulting
symptoms are ultimately correlational. (With HIV the authors fail to assert that this
correlation is strong; virtually everyone infected with HIV develops AIDS-like
symptoms within 10 years.)
HIV may not be the cause of AIDS, but the overwhelming body of evidence tells
us otherwise. Suggesting, as the authors do. that the government is standing in the
way of finding the real cause of AIDS given the amazing lack of evidence for such
a statement is irresponsible. The authors should not have made it. and Reason
magazine should not have printed it.
Mark W. Nowak
The epidemiologic, laboratory, and clinical evidence that HIV is the cause of AIDS
is overwhelming. This evidence has been used as a basis for national and
international prevention programs and clinical and vaccine trials.
Thomas et al. mix fact with fiction to misinform readers. For example, the authors
suggest that AIDS cases are an artifact of the CDC's AIDS surveillance case
definition, that there are "thousands of cases of AIDS without HIV," and that "such
cases tend to disappear from the official statistics."
The AIDS surveillance case definition was not designed to prove the existence of
HIV. However, it provides additional evidence to what epidemiologic and
laboratory studies have already told researchers- -that HIV causes AIDS. Case
definitions of any disease or health condition are basic tools of public health
surveillance. They are devised by epidemic investigators in response to clusters or
outbreaks of new or unusual health phenomena. The first CDC AIDS surveillance
case definition was developed in response to clusters of patients with unexplained
opportunistic infections and Kaposi's sarcoma in 1981. Patterns identified from
early case reports provided convincing evidence that the new syndrome was caused
by an infectious agent. This definition has been expanded three times (in 1985,
1987, and 1993) in response to greatly increased knowledge of the
immunopathology and health effects of HIV infection; each expansion served to
encompass more persons with symptomatic HIV infection. Thus, far from being an
artifact, the CDC's AIDS surveillance case definition is what it was intended to be-a
tool to track the many persons in the latter stages of HIV infection.
The authors claimed that there are "thousands of cases of AIDS without HIV." A
small percentage of cases reported to CDC have been in patients who have never
had an HIV antibody test. The majority of these cases were diagnosed and reported
before the first HIV antibody test was licensed in 1985. These cases were
diagnosed based on the presence of "indicator" diseases (mainly Pneumocystis
carinii pneumonia and Kaposi's sarcoma) that are very rare in immunocompetent
persons not infected with HIV. In addition, their supposition that these cases were
further defined as idiopathic CD4+ T-lymphocytopenia (ICL) is not true.
Investigations show that ICL cases and AIDS cases differ epidemiologitally. Thus
far, researchers have found that ICL is rare, and that no more than 100 of these
AIDS cases do not disappear. Missing or incomplete information that accompanies
AIDS cases reported to CDC through state health departments is often updated.
Most cases reported without risk information are reclassified as follow-up
investigations are completed.
The inevitable conclusions of more than a decade of research are that most people
exposed to HIV through sexual contact, injecting drugs, or transfusions are
susceptible to HIV infection. Nearly all persons who become infected with HIV will
eventually develop AIDS.
Surveillance data have been useful in developing prevention and control programs
for persons at risk of HIV infection. AIDS prevention programs continue to be
based on our understanding of scientifically defined HIV transmission modes
because prevention of AIDS is prevention of HIV. To deviate from or ignore this
concept would result in an unconscionable tragedy.
Brenda W. Garza
D. Peter Drotman, M.D., M.P.H.
Harold W. Jaffe, M.D.
Division of HIV/AIDS
National Center for Infectious Disease
Centers for Disease Control and Prevention
"What Causes AIDS?" contains misleading and incorrect information questioning
the contagious nature of HIV infection and its causal role for AIDS. This has
serious consequences, as this infection almost invariably results in long, painful,
terminal illnesses and death. The authors are distinguished in fields far removed
from the epidemiology of HIV and AIDS about which they pontificate. Would any
of your readers hire an electrician to repair a faulty toilet?
The authors assert, "The only evidence that HIV does cause AIDS is correlation."
Correlation has established the causes of many diseases: smoking and lung cancer,
Staphylococcus aureus infection and toxic shock syndrome, and ionizing radiation
and leukemia, to name a few. They state, "There are many cases of persons with
all the symptoms of AIDS who do not have any HIV infection." This is not
surprising as immune suppression, the underlying cause of AIDS, may result from
defective genetic mechanisms, toxic chemical exposures, medicinal treatments, and
infections other than HIV. They also assert, "There are also many cases of persons
who have been infected by HIV . . . and show no signs of illness." About half of all
HIV-infected persons develop AIDS within 10 years and of these, 90 percent are
dead within two years. In studies observing HIV-infected persons for more than 10
years, over 85 percent have developed AIDS.
The authors claim that the San Francisco Men's Health Study, for which I am
"principal investigator," was "designed not to test the HIV theory but to measure
the rate at which HIV-positive gay men develop AIDS. They did not compare
otherwise similar persons who differ only in HIV status, did not control effectively
for drug use, and did not fully report the incidence of AIDS-defining conditions in
the HIV- negative men." These assertions are misleading or just plain false.
The San Francisco Men's Health Study is an epidemiological investigation of the
cause or causes of AIDS, its transmission, and the natural history of the disease.
Participants were a random sample of 1,000 single men living in AIDS-affected
areas of San Francisco in 1984. When a serological test for HIV infection became
available in late 1984, the participants were tested to determine HIV-infection
status. This allowed the investigators to conduct a large number of important
analytic studies of causal factors, modes of transmission, and the natural history of
HIV infection and AIDS.
An analysis of drug use, AIDS incidence, and progressive immune deficiency, using
appropriate statistical techniques and proper controls, was published in 1993. No
relationship between drug use and AIDS incidence or immune deficiency
progression was found. The advocates of the drug etiology of AIDS have never
accepted these findings nor the findings from several other rigorous studies of the
Because an AIDS diagnosis is almost invariably followed by death within two
years, deaths may be substituted for AIDS diagnoses to evaluate the occurrence of
cases among the uninfected. In the San Francisco Men's Health Study, 581
participants, who were uninfected by the HIV on entry, remained uninfected for
over eight years. Among them, eight deaths occurred, for a cumulative rate of 1.4
percent. Of the 400 men infected by the HIV, 169 deaths Occurred, for a
cumulative rate of 42.3 percent. These data are inconsistent with the contention
that there were AIDS cases among the uninfected.
Space precludes a complete refutation of the other misstatements which burden the
article. The readers of Reason magazine should not be misled about the
consequences of HIV infection. As indicated above, these consequences are very
serious. Regardless of whether or not HIV infection causes AIDS, it is a strong
predictor of premature death.
Warren Winkelstein Jr., M.D., M.P.H.
Professor of Epidemiology (emeritus)
School of Public Health
University of California
It has now been over three years since I first challenged Peter Duesberg and a
co-writer that if they really don't believe HIV causes AIDS they should publicly
inject themselves with the virus. It would hardly be the first time a doubter of a
pathogen-disease hypothesis has intentionally exposed himself. Nevertheless,
Duesberg and fellow have steadfastly refused to do so and neither have any of
Duesberg's vocal followers volunteered to take their place. They won't shoot up,
but as their article "What Causes AIDS? It's An Open Question," shows, they won'
t shut up, either.
To address just a few major points:
They write that "after spending billions of dollars, HIV researchers are still unable
to explain how HIV, a conventional retrovirus with very simple genetic
organization, damages the immune system, much less how to stop it."
Only three retroviruses have been discovered, the first barely over a decade ago.
How does one become "conventional"? The authors want us to believe that
because it is "conventional" and simple genetically it should have been cured by
now, but all viruses are genetically simple and we have cures for none of them.
What will make curing HIV all the harder is that it is so very unconventional in that
unlike any other human virus we know about, it attacks the very immune system
and to date our disease-fighting tools have always relied on the immune system as
As to how it damages the immune system, there are numerous medical journal
articles on the subject, the latest in the June 2 issue of Nature. This doesn't mean
we understand how HIV works in the same way that we understand, say, internal
combustion in a piston engine. Human physiology is infinitely more complicated
than a motor. Still, we certainly know more about the actions of HIV than we do
about most viruses simply because HIV has been so heavily studied. Finally on this
point, knowing the cause and knowing the cure may have little or no relationship.
For hundreds of years, people knew that cigarette smoking caused lung cancer, yet
the cure rate for lung cancer even today is dismal.
The authors state, "In the absence of any agreement about how HIV causes AIDS,
the only evidence that HIV does cause AIDS is correlation. " Aside from ignoring
the medical literature, they fail to recognize that epidemiology has always been
about correlation. Long before there were electron microscopes, cell lines, and the
National Institutes of Health, epidemiologists were identifying diseases and saving
millions of lives from them based strictly on careful observance of who was getting
sick and why. Walter Reed didn't have the least idea of what yellow fever did on a
cellular level, but he saw that it was transmitted by mosquitoes and he was thus
able to practically eliminate it. Edward Jenner developed the first anti-viral vaccine
a century before anyone knew what a virus was.
The conspiracists cavalierly dismiss the San Francisco study, reported on in Nature,
along with the Vancouver one, reported on in the Lancet, without providing any
detail on them. Here is a brief summary of the San Francisco one. Researchers
directly tested the Duesberg thesis 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 and were negative for HIV with homosexuals who were heavy drug users
who were both positive and negative for the virus. Reporting their results in the
March 11, 1993 issue of Nature, they found that among homosexuals who were
sero-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
heterosexuals, less than 1 percent had died and none had gotten AIDS. In addition
to devastating the drug-use-causes-AIDS thesis, this study showed as close a
correlation between pathogen and disease as one could ever hope to attain.
All this means nothing to the REASON authors. Forget those studies; they weren't
set up to our exact specifications, they say. No, and none ever could be. Besides,
they say, "the main point they supposedly prove has already been thoroughly
disproved: AIDS does occur in HIV- negative persons." But no, it doesn't,
Certainly one can get diseases that resemble AIDS, just as one can get a disease
that resembles the flu. (How often do we hear of someone suffering a "flu-like
illness" ?) A chronic cough and expectoration of blood can be symptomatic for
bronchitis, tuberculosis, or lung cancer. It doesn't mean these are all the same
disease. As the authors themselves point out, the definition of AIDS symptoms
covers a wide area. Certainly, it's not difficult for other diseases to mimic that
which some AIDS patients may be suffering. This doesn't make them AIDS cases
any more than a bloody cough makes TB be lung cancer.
Among hundreds of thousands of sufferers of any given disease there will be a
tremendous spectrum in manifestation of symptoms and plenty of anomalies, but
with HIV there is a strong pattern of disease progression. After a few years of
infection persons begin to lose T-helper cells, then begin to develop outward
manifestations of immune dysfunction such as oral candidiasis, then begin to suffer
life-threatening diseases such as pneumocystis carinii pneumonia. Outside of
persons given immune-suppressing drugs, PCP is remarkably rare, so much so that
prior to the AIDS epidemic the CDC was dispensing fewer than 100 proscriptions
of pentamidine (at that time the only treatment for the disease) a year. In 1993,
however, there were over 12,000 confirmed PCP diagnoses and another 7,000
suspected cases, all in HIV-positive persons. In other words, if you don't have HIV
your odds of getting PCP are one in several millions. If you do have it, your odds
before the introduction of aerosolized pentamidine as a preventative treatment were
better than 50-50. Even now, they may be better than one in four. What an
HIV cohorts have shown that after about 10 years of infection, half of all persons
will be dying while almost all of the rest will be suffering severe symptoms. The
authors make much of the fact that some HIV carriers remain healthy even after 11
years of infection. As always, they ignore the rule for the exception, making us
think the edge of the bell curve is the top. Probably no pathogen known kills with
100 percent efficacy; indeed, about 90 percent of persons carrying the bacteria that
causes tuberculosis will never manifest the disease. An even smaller percentage will
suffer symptoms from infection with cytomegalovirus. Indeed, the correlation
between HIV and manifestation of symptoms, and the correlation between HIV
and death, may prove to be stronger than that for any pathogen present in the
Much of what the authors say is unquestionably true, and just as unquestionably
doesn't support their case.
Certainly there are co-factors that increase the rate at which HIV decimates the
immune system, co-factors that if blocked might greatly increase the length and
quality of life for persons with HIV. Co-factors commonly play a role in disease
causation. But nobody says that because mycobacterium tuberculosis appears to
work with co-factors to manifest as TB that mycobacterium tuberculosis isn't the
cause of the disease. The reason? Because you can have those co-factors, but
without the mycobacterium, you don't get TB. Just so with HIV and AIDS.
Further, quite the opposite of what the Duesberg conspiracists would have us think,
scientists have already been devoting a tremendous amount of research to finding
HIV co-factors, albeit with precious little to show for the effort.
And yes, certainly the African AIDS epidemic has been overstated, with every fatal
disease under the African sun being dubbed AIDS because that seems to be the
only disease Westerners care about. But this does nothing to support the
conspiracists' hypothesis. Likewise, I was writing about-and staking my reputation
on-the exaggeration of the American epidemic, especially with regards to
middle-class heterosexuals, long before the authors published word one on the
subject. I did so by analyzing patterns of both cases and infections. I noted in 1989
that since stored blood samples indicated that HIV infections appear to have peaked
out in American cities around 1981 and 1982 and since it takes on average about
10 years for an AIDS infection to manifest, the epidemic wits probably on the
verge of peaking. Indeed, the CDC noted recently (to the deafening silence of the
media), that using the pre-1993 definition of the disease, AIDS cases did decline in
Of course I have now become one of the AIDS conspirators-that group of persons
so callous and vicious that we are willing to let hundreds of thousands of Americans
alone die of this horrible disease. That or I've just closed my mind like a steel trap,
like John Maddox supposedly has. "Like other leaders of the scientific
establishment," write the conspiracists, "Nature editor John Maddox is fiercely
protective of HIV theory. He indignantly rejected a scientific paper making the
same point as this article."
In fact, toward the end of Rethinking AIDS, a Duesberg conspiracy book, author
Robert Root-Bernstein crowed: "John Maddox . . . has written that he should have
given critics of the HIV theory, such as Peter Duesberg, room to express their
concerns." So he did. It was only after the aforementioned 1993 Nature article,
along with two other Nature articles discussing how HIV causes AIDS, that
Maddox editorialized, "Duesberg, having led many people with AIDS on a
seductive path, should now admit the likelihood that he is mistaken."
But like the AIDS alarmists against whom they have rightly aligned themselves,
neither Duesberg nor his acolytes are ever going to let a little thing like scientific
evidence get in the way.
St. Petersburg, FL
(Michael Fumento is the author of "The Myth of Heterosexual AIDS.)
Charles A. Thomas Jr., Kary B. Mullis, and Phillip E. Johnson reply:
Many things have happened since our article was written, all of them supportive of
our position. Here are some highlights:
1) Harvard Professor Bernard Fields published a commentary in Nature that
signalled, in the words of The New York Times, that "a new consensus has
emerged among many leading scientists that the nation's $1.3 billion AIDS research
program is on the wrong track." Planned trials of candidate vaccines have been
abandoned as unpromising and dangerous because, according to Fields, "We still
have too many serious gaps in our fundamental knowledge to know how to prevent
and treat AIDS, and must return to a broader base to study the scientific questions
The primary gap, of course, is the absence of anything but speculation to explain
how an ordinary retrovirus can be killing billions of immune cells that it doesn't
even infect. (That the PCR technique can find genetic sequences associated with
HIV-not active virus-in lymph nodes does nothing to solve the mystery.)
Unfortunately, Fields's back-to-the-drawing board stance, which has been endorsed
by top NIH officials, does not imply any real reconsideration of the HIV dogmas
that have brought the re searchers to this dead end. It means only that some of the
All)S money will be diverted to general biochemical research that is only
tangentially related to AIDS.
2) Another Harvard professor and member of the HIV inner circle, Max Essex,
published with African colleagues a paper in the Journal of Infectious Disease
detailing an extremely high incidence of false positive results among both leprosy
patients and their uninfected neighbors on HIV antibody tests. In a group of 57
leprosy patients, for example, 70 percent tested positive for antibodies but more
extensive testing confirmed the presence of H IV in only 2 patients. The paper
concluded that, due to an unexpectedly high rate of false positives on both the
ELIZA and Western Blot tests, these standard antibody tests "may not be sufficient
for HIV diagnosis in AIDS-endemic areas of Central Africa where the prevalence
of mycobacterial diseases is quite high." These results clearly call into question all
projections about HIV infection in Africa and elsewhere that are based on antibody
Antibody tests may be more reliable as an indicator of HIV infection in relatively
healthy groups like U.S. Army recruits. Our critics misunderstand this subject,
however. Both the ELIZA arid the Western Blot are antibody tests, not tests for
active, replicating virus. Both have also been shown to cross-react with things other
than HIV antibodies. To say as Daniel Cosgrove does that the "HIV antibody test"
is confirmed by the Western Blot in many cases is merely to say that two faulty
antibody tests have produced consistent results.
3) A study by Mulder et al. for the British National Research Council (published in
Lancet) has been misleadingly cited by CDC officials and others as proof that a
pandemic, caused by HIV, is raging through Africa. The study actually does show
that, in a Ugandan village population, persons registering positive on the antibody
test had a much higher death rate than antibody-negative persons, especially in the
age group 25-34. What the HIV propaganda does not say is that the subjects did
not die of AIDS. Of 64 deaths of persons aged 25 to 34, only 5 were diagnosed as
AIDS under the very broad "Bangui" (African) definition, which requires only
conditions like sustained weight loss and persistent diarrhea. Severely diseased
persons are likely to have many microbes in their system, including HIV and other
things that produce positive results on the inaccurate antibody tests. That this study
of non-AIDS deaths was claimed to support the HIV theory of AIDS and the
existence of an African AIDS pandemic is eloquent testimony to the closed mindset
that rules the HIV research community.
4) A conference on nitrite inhalants (poppers), held under the auspices of the
National Institute on Drug Abuse in May 1994 was attended by such HIV kingpins
as Robert Gallo and Harold Jaffe-and dissenter Peter Duesberg. Participants
acknowledged that the data do not support the claim that HIV is the sole or even
the primary cause of Kaposi' s sarcoma (KS) in gay males. This concession is
particularly remarkable because KS is still officially one of the prime AIDS-defining
conditions, and many gays with KS have been classified as having "HIV disease"
on "presumptive" criteria that do not require antibody testing.
The problem with the HIV/KS hypothesis is that there are dozens of known cases
of KS in young gay males who have never been HIV infected, and KS is very rare
among non-gay HIV positives. Even the HIV stalwarts now admit that the primary
cause of KS must be some agent that is specific to gay men, such as a
still-undiscovered sexually transmitted microbe specific to gays, or poppers. Thus
while evidence pointing to poppers as a causative factor in KS is ridiculed by the
HIV propagandists, the research community is increasingly finding the evidence
impossible to ignore.
5) Mounting evidence indicates that what is called "AIDS" in hemophiliacs is
caused not by HIV but by the (curable) effect of foreign proteins from treatment
with unpurified Factor 8, the blood coagulant that saves hemophiliacs from an early
death due to prolonged internal bleeding.
The way the good news about hemophiliacs is expressed in an HIV-obsessed
research culture is by lengthening the "latency period," a statistical fudge-factor that
is different in every risk group and can be adjusted as necessary to explain why so
many HIV-positive people are not sick. A recent British study of 111 hemophiliacs
showed that so many fewer than anticipated are suffering immune system failure
that 25 percent are predicted to be "AIDS free" for 20 years or more.
What is helping hemophiliacs to avoid immune deficiencies is not harmful and
ineffective antiviral drugs, but new purified blood products that do not contain
foreign proteins. Highly purified Factor 8 has proved so effective in protecting the
immune systems of hemophiliacs that some HIV-minded researchers are thinking
of employing it against " HIV disease" in non-hemophiliacs. (Complete details on
the hemophiliac studies are provided in a forthcoming paper by Duesberg in
This use of the latency period (and mysterious "genetic immunity") to explain away
the many healthy HIV positives explains, by the way, why it would prove nothing
for Duesberg or anyone else to inject himself with the virus and survive. If he lived
50 years longer and died at 110, HIV science would conclude only that the latency
period is sometimes unusually long, or perhaps that Duesberg was one of the lucky
folk with genetic immunity. (As for ourselves, we stick to scientific evidence and
have no interest in showmanship.)
We find a similar use of this convenient fudge factor in Daniel Cosgrove' s
argument that the latency period accounts for why nearly 90 percent of AIDS cases
are still male in North America and Europe, despite changes in the definition of the
syndrome aimed at including more women. That excuse gets thinner every year as
confident predictions based upon the "everyone is at risk" ideology fail to come
true. We quote again the important finding of the National Research Council: "The
convergence of evidence shows that the HIV/AIDS epidemic is settling into
spatially and socially isolated groups and possibly becoming endemic within them."
This is the opposite of what the HIV theory predicted.
6) The Tenth Annual International AIDS Conference in Yokohama in August 1994
was the last of its kind. The annual gathering of the multitudes who make their
living from HIV will be skipped next year, because HIV science is at a virtual
standstill and there is nothing of importance to announce. The great breakthrough
touted in Yokohama was a study claiming a reduction in the rate of infant HIV
infection when expectant mothers and babies were given AZT. The study was
terminated abruptly, as has happened with earlier AZT studies that began to show
favorable results at an early stage.
In consequence a highly toxic drug that is known to be ineffective and positively
harmful in antibody-positive adults will be given routinely to unborn and newborn
infants with antibody-positive mothers, although most of these infants would never
be HIV infected anyway. The uncertain benefit and great risk would make such a
reckless course of conduct unimaginable in normal circumstances, but the AZT
lobby backed by HIV hysteria has the power to overrule the prudent standards that
protect the public from other dangerous and unproven drugs.
What the Yokohama conference lacked in science it more than made up in scare
stories and plans for worldwide social engineering to protect Asia and Africa from
depopulation. (As Tom Bethell says, AIDS is not so much a disease as an
open-ended government program.) The media as usual reported uncritically the
claims that HIV infection is increasing rapidly everywhere in Asia and Africa and
that the relatively low number of AIDS cases actually reported is just the tip of the
What the media did not report is that the same virus that is supposed to be newly
infecting millions of people every year in regions where reliable statistics are hard to
come by has been stable in the U.S. population ever since testing began, almost 10
years ago. Every year the AIDS agencies ominously report that "I million people
are now infected with HIV," and the reporters never point out that the figure was
exactly the same the year before and the year before that. We call upon the CDC
to confirm or deny what The New York Times reported months ago-which is that
the most reliable studies show that the actual total number of antibody-positive
Americans is well under one million, and not rising. The thoroughly researched
American figures utterly contradict the inflated claims about HIV infection rates in
Asia and Africa-unless we indulge the kind of racist speculation about non-white
sexual habits that Charles Geshekter rightly denounces in his letter.
As one of us (Mullis) has frequently commented, there is no paper in the scientific
literature that reviews all the relevant evidence and establishes that HIV is the cause
of AIDS. George Fergus to the contrary notwithstanding, the original papers
announcing the discovery of HIV in 1984 said only that HIV had been found in
some (not all) of a small group of AIDS patients. No proof was presented, but Dr.
Gallo and his fellow virologists seemed so confident that the research community
wrongly assumed that they had the proof. Once that assumption was set in
concrete as the foundation for funding, critics could no longer be tolerated.
Instead of a paper that takes the objections seriously and undertakes to prove the
point at issue, we find only polemics that assume the HIV theory and defend it
against specific criticisms with question- begging arguments. Mark Nowak, for
example, says that the failure of HIV to cause AIDS in the many chimps who have
been deliberately infected with the virus says nothing about whether HIV causes
AIDS in humans. Our point was that one of the recognized ways of proving that a
virus does cause a disease in humans is to cause the disease in animals by infecting
them with the virus, and such efforts have failed with HIV. The chimps do get HIV
infection, just like humans, and HIV does no damage to their immune systems.
Why not? To say as Mark Nowak and the HIV scientists do that "HIV does not
cause AIDS in chimps" is merely to restate the question.
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
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-de-fining 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
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
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. *