the Reason article- What Causes Aids?
WHAT CAUSES AIDS?
The debate continues
Reason, Dec. 1994
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
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.
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.
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 reconfigure
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.
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
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 gathering.
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.
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.
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.
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
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
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.
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 either.
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.
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.
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.
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 AIDS.
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.
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."
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.
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.
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 cases exist.
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.
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.
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.
Drotman, M.D., M.P.H.
W. Jaffe, M.D.
Center for Infectious Disease
for Disease Control and Prevention
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?
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.
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.
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 drug hypothesis.
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.
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.
Winkelstein Jr., M.D., M.P.H.
of Epidemiology (emeritus)
of Public Health
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.
just a few major points:
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."
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 an ally.
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.
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.
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.
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 amazing coincidence.
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 human population.
Much of what
the authors say is unquestionably true, and just as unquestionably
doesn't support their case.
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 1992.
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.
Fumento is the author of "The Myth of Heterosexual AIDS.)
A. Thomas Jr., Kary B. Mullis, and Phillip E. Johnson reply:
have happened since our article was written, all of them supportive
of our position. Here are some highlights:
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 confronting us."
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.
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 testing.
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
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
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
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
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 Genetica. )
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.
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 iceberg.
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.
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.
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.
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.
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.
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 other
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.
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
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.
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.
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.