Kangaroo Court Etiology

by John Lauritsen

[Please note: This article was published in the New York Native (9
May 1988), and was reprinted as Chapter XII of the book, POISON BY
PRESCRIPTION: THE AZT STORY (ny 1990). I hereby give permission to
print out this document and to photocopy it. However, it may not
be published commercially without my permission. — John Lauritsen,
Box 1902, Provincetown, MA 02657-0245. E-mail: jlaurits@capecod.net]


A “Scientific Forum on the Etiology of AIDS”, sponsored by
the American Foundation for AIDS Research (AmFAR), was held on
April 9, 1988 at the George Washington University in Washington,
D.C. In the words of the AmFAR “fact sheet”, the Forum was
“convened to critically examine the evidence that human
immunodeficiency virus (HIV) or other agents give rise to
the disease complex known as AIDS. Data from laboratory,
clinical, and epidemiological research will be presented and
evaluated. The forum seeks no consensus, instead it is
designed to permit discussion among experts on the
conclusions the facts permit.”

As one of the 17 journalists who attended, I looked forward
to the forum as the first opportunity for an open discussion of
the pros and cons of the hypothesis that HIV is the cause of
AIDS. Ever since Secretary Heckler announced in 1984 that the
cause of AIDS had been discovered, HIV has been accepted as the
cause despite the lack of proof that it is. The Public Health
Service and the rest of the medical establishment have acquiesced
in a “Proof by Proclamation”. The forum offered the first
opportunity for Peter Duesberg, Professor of Molecular Biology at
the University of California at Berkeley, to confront members of
the “AIDS establishment” over their HIV hypothesis. Over a year
ago Duesberg provided a comprehensive and cogently argued
refutation of the HIV hypothesis, to which the “AIDS
establishment” has intransigently refused to reply (New York
Native 220).

Despite these praiseworthy intentions, the forum appears to
have had a hidden agenda: to discredit Duesberg. Even Michael
Specter, a reporter who caters to the “AIDS establishment” and is
bitterly opposed to Duesberg, admitted that the April 9 meeting
“was billed as a scientific forum on the cause of AIDS but was
really an attempt to put Duesberg’s theories to rest.”
The forum represented several steps forward, and several
backward. At least the ice has been broken, and the causes of
AIDS are now an acceptable topic for public discussion. While no
blows were struck, some of the HIV protagonists fell below the
standards of civility that are expected in scholarly debate.
Nothing particularly new was said, and there was little of the
give and take that characterize genuine scientific dialogue. At
the same time, the positions of both sides have become more
sharply defined; it is now clear what directions future debate
should take.

On the whole, I regard the forum as a victory for Duesberg.
The forum was a well-orchestrated media event, heavily stacked
against him, and he took a lot of abuse. Nevertheless, he stood
by his guns; he did not recant (as he apparently was expected
to); and to the more discerning participants, he exposed the
bankruptcy of the arguments currently advanced in favor of the
HIV hypothesis. At all times Duesberg retained good manners and
a sense of humor, in the face of invective, insults, and clowning
from his opponents.

Before going into what each of the panelists said, I’d like
to discuss a couple of general issues which came to the fore:
Koch’s Postulates and the nature of scientific evidence.

Koch’s Postulates

The forum was haunted by the specter of Robert Koch, and the
postulates that he formulated for “establishing the specificity
of a pathogenic micro-organism”. For a century, medical science
has used Koch’s postulates as the standards for proving that a
particular micro-organism causes a particular disease. The first
Postulate requires that the microbe be found in all cases of the
disease; the second, that the microbe, having been grown in pure
culture, be injected into susceptible animals with the result
that the same disease is produced; and the third, that the
microbial agent create the disease upon transfer from animals
made ill by inoculation.

Duesberg has taken the position that Koch’s first Postulate
should be amended in a conservative direction, so that the
microbe must not only be present in all cases, but must also be
biochemically active to a clinically relevant degree. His
rationale is that present-day technology makes it possible to see
viruses that would have remained unknown and undetectable only
ten years ago. It is now possible to identify a virus that is
present in only one in 100,000 T-cells. So it is not enough to
detect a microbe; it must be proven that the microbe is doing
something harmful, and to a sufficient degree, that illness
results. Duesberg has also commented, that if Koch’s first
Postulate is not satisfied, there is no need to bother about the
remaining postulates.

The HIV advocates, on the other hand, now wish to revise
Koch’s in a more permissive direction: it would no longer be
necessary to find the microbe in all cases of the disease. Mere
correlations between microbial antibodies and the progression of
the disease would be sufficient. HIV could be proved
“epidemiologically” to be the cause of AIDS.

Actually, the HIV advocates talked out of both sides of
their mouths with regard to Koch’s postulates. On the one hand,
they disparaged them as in need of “modification” (read:
abandonment); on the other hand, they were doing their best to
come up with data that would satisfy at least the first
postulate, which is troublesome because it amounts to good common
sense.

Public vs. Private Facts

Duesberg has based his critique of the HIV hypothesis on a
thorough review of the published literature on AIDS. In the
course of the debate, it appeared that the HIV advocates are
trying to shore up their arguments by revising the facts,
particularly with regard to the crucial questions of whether or
not HIV is ever biochemically active in people with AIDS (PWAs),
and whether or not HIV can be detected in all PWAs.
Several times Duesberg was accused by Anthony Fauci and
William Haseltine of having based his arguments on research that
was “out of date”. Duesberg replied that some of the key figures
he cited had been used recently by members of the AIDS
establishment, and that he looked forward to reading reports of
any new data.

A fundamental difference in philosophy is involved here, one
which needs to be articulated. On several occasions Duesberg and
Harry Rubin, Duesberg’s colleague at Berkeley, asked Fauci or
Haseltine for references to back up assertions they had made, and
they were rudely rebuffed. Both Duesberg and Rubin belong to the
old school, according to which facts are not entirely “real”
until they have been published. Scientists are expected to make
their data available, together with a detailed description of
methodology, so that other scientists, working independently,
could attempt to replicate the experiments and verify the
results. Science is thus a public activity, where scientists
check out each other’s work in a mutual endeavor to establish the
truth.

Unfortunately, government scientists and others in the AIDS
establishment have sometimes been motivated by considerations
other than the truth. In the interests of profit, prestige, and
public relations, they have resorted to secrecy and deception. A
case in point is the well-documented episode in which Robert
Gallo attempted to steal credit from the French for the discovery
of the “AIDS virus”.

The difference in philosophy needs to be emphasized.
Duesberg, basing his arguments on public facts, was countered by
Fauci and Haseltine, who referred to their own private facts.
Now, it is possible that Duesberg’s public facts may be wrong,
and that Haseltine’s and Fauci’s private facts may be correct.
But even if that were the case, it would be a grave injustice to
Duesberg to criticize him for having used public information.
When Duesberg insists upon references, he is not quibbling; he is
acting in the best tradition of science.

Harold Ginsberg

The panel was moderated by Harold Ginsberg, Professor of
Medicine and Microbiology at Columbia University. He began by
saying that recording of the forum would not be permitted,
although there would be an official transcript of the
proceedings, and that the purpose of the forum was to “discuss in
an informal and friendly manner the etiology of AIDS.” He then
went into a presentation of his own. After conceding that “the
pathogenesis of HIV is still pretty much a black box”, he
discussed the characteristics of several viral diseases,
including influenza, poliomyelitis, measles, herpes simplex, and
hepatitis B. He emphasized that neutralizing antibodies could be
present when disease occurs, and did not necessarily prevent
viruses from being present in the blood.

Ginsberg’s comments served to set the stage against Duesberg
by toppling a straw dummy representing selective statements, torn
out of context, which Duesberg had made on antibodies. It became
obvious that the forum would not favor free and impartial
discussion of the issues — an impartial discussion, after all,
requires an impartial moderator. It was also obvious that the
HIV protagonists would employ information overload as a
propaganda technique. While Ginsberg’s comments were true
enough, so far as they went, they were mostly irrelevant to the
central issues of the debate. Nevertheless, they conveyed the
impression that a vast body of knowledge argued against
Duesberg’s critique of the HIV hypothesis. Novice reporters,
straining to take in all of Ginsberg’s information (without the
aid of tape recorders), ended up with little space in their heads
for the relevant issues.

Marcel Beluda

The next speaker was Marcel Beluda, Professor of Pathology
at the University of California at Los Angeles. His presentation
dealt with the complex structure and reproduction cycles of
retroviruses, and what rules a retrovirus would have to follow in
order to cause disease. He said that, with regard to Koch’s
first Postulate, retroviral DNA should be present in 100% of the
cases, and that it was a serious weakness in identifying HIV as
the etiological agent that this requirement could not be
satisfied.

Beluda’s presentation was complex and highly nuanced, and he
ran out of time. Nevertheless, his concluding statement came out
clear and strong: “We must resolve the ‘black box’ HIV biological
phenomenon.”

Harry Rubin

Harry Rubin, Professor of Molecular Biology at the
University of California at Berkeley, was one of the pioneers in
the field of retrovirology. Twenty years ago Rubin was king of
the field; he trained many of the scientists who are today the
world’s leading retrovirologists.

Rather than discussing the intricacies of molecular biology,
Rubin went instead to the heart of the matter: the conceptual
problems of AIDS. Rubin said that he was disturbed by the
simplicity of the causal explanation that had been put forward.
An enormous complexity of disease states constitute the AIDS
Syndrome; no fewer than 20 different diseases are classified as
“AIDS”. Cartesian reductionism — the notion that complex
phenomena can be reduced to a single cause — didn’t make much
sense in this context. The simplistic notion of a single disease
entity caused by a single virus ignored the role played by the
condition of the host — the complex, life-long interaction
between the host, the environment, and microbes.

For Rubin a red flag went up when he learned that Burkitt’s
lymphoma was classified along with the many other manifestations
of AIDS. He recalled that for many years attempts had been made
to explain Burkitt’s lymphoma and other cancers in terms of
viruses, with such candidates as Epstein-Barr virus proposed.
The generally favored explanation came to be chromosomal
abnormalities. And now, apparently, “HIV infection” is supposed
to be a cause of some cancers.

Rubin said that the simplistic HIV causal explanation raised
a lot of questions, and recalled a theory that was popular 20
years ago to explain the origin of cancer. The “immune
surveillance theory” held that the body somehow lost its immune
capacity and, in consequence, its ability to hold down cancers.
The theory is no longer talked about owing to experiments on
athymic mice, known as “nude mice”. (Lacking thymus glands, nude
mice cannot manufacture T-cells, and therefore lack a cellular
immune system.) What dissolved the “immune surveillance theory”
was the discovery that nude mice, while susceptible to many
different diseases, had no higher incidences of any cancer than
did mice with normal immune systems. So, Rubin asked, how can we
talk about “immune deficiency” as being responsible for the
cancers that are considered to be a part of the syndrome known as
“AIDS”?

Rubin concluded by saying that he found any single cause of
the enormous complex of diseases to be seriously inadequate.
While he was not willing categorically to rule out the
possibility that HIV might play some role in some cases, he was
“not ready blandly to accept it as the single cause of all of the
disease complex.” Rubin posed the question, to what extent is
the virus itself an opportunistic infection? He found it
irresponsible to focus exclusive attention on the putative viral
cause while failing to address the associated practices of high
risk groups (heavy use of recreational drugs, overuse of
antibiotics, promiscuous sexual behavior) which are themselves
known to compromise the immune system.

In the question period following Rubin’s presentation,
William Haseltine bluntly challenged Rubin on the issue of high-
risk behavior, and asserted that the best correlation with AIDS
is “evidence of viral infection”, and that there were many
instances of AIDS in persons with no known risk factors. Rubin
replied that the serological evidence seemed to argue against
HIV, since in many PWAs neither antibodies nor virus could be
detected.

Beluda then intervened, apparently annoyed by Haseltine’s
belligerence, to state that sometimes even a single exception is
sufficient to disprove a theory. HIV antibodies are reportedly
found in 90% of PWAs, but what about the other 10%? “This is the
crux of the matter”, Beluda said, “the virus cannot be found in
all cases of AIDS.”

Fauci responded to Beluda by saying that a “good lab” was
able to isolate the virus in 90-100% of the cases, that there was
“no question about it”. Fauci did not provide a reference to
published data, nor did he indicate what the “good labs” were, or
how exactly they differed from the not-so-good labs.

Peter Duesberg

(Since Duesberg’s presentation covered a lot of ground, I’ll
try to summarize just the main points here. To understand the
full scope of his arguments, the articles listed below under
“References” should be consulted.)

Basically Duesberg argued that HIV does not have the
physical properties to cause disease, let alone the devastating
pathology associated with AIDS. The HIV hypothesis is fraught
with contradictions (or “paradoxes”); it violates the rules that
all other microbes follow when they cause disease; indeed, the
hypothesis sometimes violates the principle of causality itself.
Duesberg began by attacking the prevailing hypothesis: that
HIV kills T-cells after a bizarre latent period of 5-8 years.

This cannot be true, he said, because retroviruses do not kill
cells — in fact, retroviruses make cells grow faster. The “AIDS
virus” hypothesis is now the basis for over $1 billion research
efforts annually, making it the most expensive virus in history.
The HIV hypothesis is the basis for the “AIDS test”, which is in
fact only a test for HIV antibodies. Antibodies, which for 200
years have been interpreted as good news, are now interpreted as
a prognosis for death. Positive results on the antibody test
have resulted in suicides and broken marriages; they would be the
basis for denying residence in China. The presence of HIV
antibodies is now being used to justify treatment with AZT, which
has one known effect: to stop DNA synthesis; the obligatory
consequence of incorporating AZT into a human cell is either a
dead or a mutated cell.

The “AIDS virus” hypothesis is based only on correlation —
between HIV antibodies and AIDS — a correlation in the
neighborhood of 80-90% (“They never say 100%”). And even if the
correlation were 100%, this would not prove causality. Further,
antibodies are not the same as the virus itself, which is so
extremely difficult to detect that only the most expensive
laboratories in the country are capable of doing so, and even
then, only in about half of the cases of AIDS.

All known viruses (polio, hepatitis, et al.) are
biochemically active when they cause disease. They have to kill
or intoxicate more cells than the host can regenerate.
Paradoxically: HIV is inactive and latent, even in patients who
are dying from AIDS. A virus cannot cause harm without doing
something. Although viruses can go through periods of latency,
neither herpes nor any other virus is inactive at the time that
it causes disease. HIV actively infects fewer than one in 10,000
T-cells, even in fatal cases of AIDS. This is trivial, the
equivalent of losing one drop of blood every day.

Viruses cause disease before, not after antiviral immunity.
This is why vaccination works. Paradoxically: HIV is said to
cause AIDS only after a peculiar latent period of 5 to 8 years.
HIV is a retrovirus, and retroviruses do not kill cells. On
the contrary, they depend on living cells to reproduce. This is
why retroviruses were the most plausible viral carcinogens in
President Nixon’s “War on Cancer”. Paradoxically: the retrovirus
called HIV is said to cause AIDS by killing T-cells. In fact,
Robert Gallo and others have observed that T-cells in culture
produce much more virus than is ever produced in AIDS patients,
yet survive indefinitely, developing into immortal lines.
No known virus discriminates between men and women, or
between heterosexuals and homosexuals. Paradoxically: even eight
years into the epidemic, AIDS shows an absolute preference for
men (92%).

The transfusion cases have been used as an argument for the
HIV hypothesis, yet transfusions do not discriminate between HIV
and all other microbes, toxins, etc. that are in the blood. That
the transfusion argument is not strong, but tenuous, is shown by
the control group of 14,000 hemophiliacs in the United States who
are antibody positive, yet only 300 (2%) of whom have developed
any of the many symptoms of AIDS. The low incidence is even more
striking in light of the fact that hemophiliacs are a
congenitally sickly population; only a few years ago, their
average life expectancy was 11 years. Furthermore, it is now
three years since the HIV antibody test came into use to screen
blood. We should have seen at least a levelling off of the
“transfusion cases”, but contrary to expectations, they have just
doubled.

According to basic logic, a virus or other pathogen would at
least have to be present when it causes disease. This is Koch’s
first postulate for identifying a causative pathogen, which
states that the presumed causative agent must be present in all
cases of the disease. However, HIV can only be isolated in 50%
of AIDS cases. Although there are unpublished observations that
the figure can be pushed up to 100%, this is not consistent with
the fact that pro-viral DNA cannot be detected in a substantial
proportion of AIDS cases. Gallo could only detect pro-viral DNA
in 15% of AIDS cases. A recent article in Science Magazine
reported being unable to detect pro-viral DNA in a significant
number of AIDS cases, even using the most sensitive techniques.
Duesberg posed the question, why is the “AIDS virus”
hypothesis so popular, in the face of so many paradoxes? He
suggested that this was due to two problems in the field:
1. Progress in biological thought has not kept up with the
rapid progress in technology. Only ten years ago, scientists
would never have detected a latent virus that is only active in
one out of every 100,000 T-cells. With their limited tools, Koch
or Pasteur or Enders or Sabin were forced to look for microbes at
clinically relevant titers. Indeed, Koch’s first postulate needs
to be amended now, in light of the technology of the present, to
state that pathogens must not only be detectable, by the most
sensitive techniques available, but must also be biochemically
active in more cells than the host can spare or regenerate.
2. AIDS is a syndrome, not a single infectious disease. The
spectrum of diseases is truly impressive… yet such things as
lymphoma and Kaposi’s sarcoma cannot be attributed to immune
deficiency, as is shown by the example of the nude mice. Nor
does immune deficiency explain dementia.
In short, the one-virus, one-disease concept is hard to
reconcile with the AIDS situation, although people would like to
see it that way. AIDS propaganda has transformed a latent, non-
cytocidal retrovirus, a “Sleeping Beauty”, into a vicious killer
virus. AIDS propaganda has reduced a complex syndrome to a
single disease entity with a single cause. What we need to do is
look at “risk behavior”, which may hold the keys to the many
diseases of AIDS.

Anthony Fauci

Anthony Fauci, Director of the National Institute of Allergy
and Infectious Diseases, has become the most publicly prominent
member of the “AIDS establishment”, often quoted in the press and
featured on television shows. His presentation, while aspiring
to be a point-by-point rebuttal to Duesberg, consisted mainly of
disconnected assertions, delivered in a tone of petulant
indignation.

Epidemiological studies conducted in San Francisco and
unpublished laboratory reports seemed to be the basis of most of
his statements. So far as I could tell, he understood virtually
none of Duesberg’s arguments; whatever else he may be, Fauci is
not a philosopher.

It is not true, Fauci said, that HIV is inactive; sometimes
there are “bursts of activity”. According to Fauci, it is false
to say that nothing is happening: HIV is “insidiously destroying
the immune system” in asymptomatic but infected people.
Fauci claimed that the AIDS virus is unique in that its
major target is the immune system itself. The disease is not HIV
infection; “it is the opportunistic infections and neoplasms that
kill the individual.” Auto-immune phenomena, etc. can also be
taken into account, in addition to the direct cytocidal effect,
which is clearly demonstrated in vitro. The macrophages can
serve as a reservoir, where the virus can hide out without being
detected by the immune system.

Fauci accused Duesberg of having said if you’re infected
this means, “hurrah, your body has won!” According to Fauci,
this flies negatively in the face of the data [based on an
unpublished San Francisco study] that within five years, 90% of
seropositive individuals will have deleterious effects on their
immune system.

Fauci countered Duesberg’s point on “discrimination” —
that the virus seems to attack mostly homosexual men — by saying
that the point was the mechanism of transmission. Risk behavior
simply meant coming into contact with the virus. He then asked a
series of abusively rhetorical questions.
“What kind of risk behavior”, he demanded, “does the infant
born of an infected mother have?”
“And what about the 50-year-old woman who received a blood
transfusion from an infected donor?”
(The answer to the first question is: 1) in the decade of
the AIDS epidemic, there have been only a few hundred reported
cases of infants with AIDS, 2) infants are not yet
immunocompetent, and 3) virtually all infants with AIDS were born
to mothers who were drug abusers — as everyone ought to know,
drugs cause birth defects. The answer to the second question is
that a 50-year old woman who requires a blood transfusion is
already at risk, and that blood transfusions involve massive
exposure to microbes, human cells, and toxins of all kinds.)
Fauci addressed the question of Koch’s first postulate by
asserting that “good labs” could find the virus in 90-95% of the
cases — that it was too much to expect 100%, because any
technique has a limitation. He concluded by saying, “The data
strongly, if not overwhelming, indicates [sic] that HIV is the
cause of AIDS.” (This is a step backward — only a few weeks
ago, Fauci found the evidence “overwhelming”.)

In the question period, Beluda asked if the evidence were
sufficient that HIV is necessary for the development of AIDS.
Fauci replied that he hoped the epidemiologists would answer that
question.

William Haseltine

William Haseltine, Chief of the Laboratory of Biochemical
Pharmacology at the Dana Farber Cancer Center of Harvard Medical
School, appeared to be an angry man. His presentation was
devoted largely to personal attacks on Duesberg, in a manner
which two of my colleagues described as “brutal” and “vicious”.
Haseltine’s anger can probably be attributed to Celia Farber’s
interview with Duesberg in Spin Magazine (January 1988), in which
Duesberg stated:

William Haseltine and Max Essex, who are two of the top
five AIDS researchers in the country, have millions in
stocks in a company they founded that has developed and will
sell AIDS kits that test for HIV. How could they be
objective?

When Celia Farber contacted Haseltine, he confirmed his and
Essex’s business arrangement with Cambridge Bio-Science, a
company that sells HIV testing kits. Said Haseltine: “I deeply
resent the implication that my business investments have affected
my work.”

Haseltine accused Duesberg of “serious confusion and
misrepresentation of fact”. He said that when rational arguments
don’t hold up, Duesberg “has resorted to personal attack; he has
impugned the motivations of individuals and institutions.”
Haseltine asserted that “HIV is demonstrably cytopathic”,
though he didn’t say how.

He quoted Duesberg as having said that antibodies were “good
news”. Not so, said Haseltine, to be antibody positive is very
bad news for the health of the individual.

Haseltine said it was not true that there was no detectable
viremia in AIDS patients, and said he would show a slide “with
the current perception with regard to viremia…during the later
course of infection, one sees rising antigenemia in most persons
infected.”

He attacked Duesberg’s “paradox”, that the AIDS virus seemed
to be able to discriminate between boys and girls, by saying that
this was not true outside the U.S. — in Africa, about equal
numbers of men and women develop AIDS. (He seemed oblivious to
the paradox that a microbe should be able to discriminate in one
country, but not in another.)

According to Haseltine, Rubin and Duesberg were confused
about nude mice, which in certain classes were capable of
“mounting a vigorous immune response”.

The most dramatic moment in the forum came when Haseltine
began showing his slides.

Haseltine’s Fake Slide

In presenting his first slide, Haseltine said, “This gives
us a summary of the virology. Dr. Duesberg asserts that during
the later phases of the disease one does not see free virus in
circulation. That is not generally reflected in the patients.
During the latter phase of the disease, the black line represents
either virus titer or viral antigens directly detectable in the
circulation. It rises later in the disease. That rise is
concomitant with the period when T-cells fall. So it is not the
case, the central assertion he has made in his arguments, that
one does not have viremia.”

At this point Duesberg asked, “Why are there no units on
that slide?”

“Don’t interrupt me”, responded Haseltine, “I didn’t
interrupt you.”

“I merely asked why the slide has no units on it”, replied
Duesberg.

Haseltine angrily refused to answer the question, and the
chairman intervened, saying that questions would have to wait
until the presentation was finished.
Perhaps Duesberg ought to have waited, but one can
understand his impatience. Witnessing a fast-flowing stream of
propaganda, he spotted something that was obviously wrong, and
wanted to confront it before the moment was lost. That his
suspicions were more than justified became clear later.
In the question period following Haseltine’s presentation,
Harry Rubin asked Haseltine if he could provide a reference for
his statement that nude mice were capable of mounting a vigorous
immune response. Haseltine said that there was a large
literature on nude mice: “If you haven’t read it, how can I
discuss it with you?”. Rubin gently replied that perhaps he had
read it, but that he had only asked for a reference.
Duesberg then requested that the slide be shown on the
screen again, and asked if it were an accident that the slide had
no units on it.

[A PHOTOGRAPH OF THE SLIDE APPEARED IN THE NEW YORK NATIVE
ARTICLE. IT SHOWS A GRAPH ENTITLED “AIDS VIRUS AND ANTIBODY”.
THE TWO VERTICAL AXES ARE LABELLED “VIRUS TITER” AND “AB TITER”,
BUT HAVE NO UNITS OF ANY KIND. THE HORIZONTAL AXIS HAS
CHRONOLOGICAL NOTATIONS WHICH ARE GIBBERISH: “3-6 WEEKS”, “2-10
YRS”, AND “1.5-2 YRS”.]

Haseltine was unable to answer the question himself, and
asked Dr. Robert Redfield of the Walter Reed Army Research
Institute, sitting in the audience, to explain how the slide was
prepared. Redfield said something to the effect that “different
measurements were used”, a grossly inadequate explanation. When
Duesberg persisted, Haseltine became truculent, and said that
Duesberg should read the literature, because there were different
measures that could be used. With no satisfactory answer
forthcoming, the chairman moved on.

The truth about the Slide Without Units came out in the
evening, at a party at the home of Dr. Harris Coulter (author of
“AIDS and Syphilis: The Hidden Link”). In a relaxed and convivial
mood, Redfield admitted, in the presence of Duesberg, Rubin,
myself, and several other witnesses, that the graph had been
prepared to illustrate a theoretical possibility. It had no
units on it for the simple reason that it was not based on any
data at all. In other words, the slide was a fake.

It is difficult to think of an innocent explanation for
Haseltine’s behavior. If he didn’t know what the slide meant, or
whether or not it was real, then he shouldn’t have used it.
Haseltine presented the slide as though it represented scientific
findings, whereas it really represented speculation. It is not
unfair to call this kind of misrepresentation, fraud. Nor is it
making too much out of one fake slide. If someone will cheat in
little things, he will cheat in big things as well. In my book,
Haseltine has forfeited his claim to scientific credibility.

Warren Winkelstein

Warren Winkelstein, Professor of Biomedical and
Environmental Health Sciences, School of Public Health,
University of California at Berkeley, gave a talk entitled
“Epidemiological Observations on the Causal Nature of the
Association Between Infection by the Human Immunodeficiency Virus
and the Acquired Immunodeficiency Syndrome”. He was the only
panelist to provide printed copies of his talk, something much
appreciated by us journalists.

Briefly, the point of Winkelstein’s presentation is that
Koch’s postulates should be superseded by new standards for
establishing the causal relationship between microbes and
disease, and that these standards should be based upon
“epidemiology”, or, as it were, correlations of various kinds.
Winkelstein and colleagues in San Francisco, under the
auspices of Fauci’s National Institute of Allergy and Infectious
Diseases, studied a sample of single men, 25-54 years of age,
over a period of three and a half years. Data were collected on
HIV antibody status over time, on progression to AIDS, and on
various other clinical parameters.

They found that none of the heterosexual males and none of
the gay men who remained seronegative developed AIDS, whereas 13%
of the men who were seropositive upon entry into the study, and
8% of those who became positive during the course of the study
developed AIDS. Further, they found that a progressive decline
in T-4 cells occurred among those who were seropositive.
They concluded that epidemiological data from their study,
together with data from a related San Francisco study (conducted
among a cohort of gay men recruited from VD clinics in 1978 for a
hepatitis B study), supported “the hypothesis of a causal
association between HIV infection and AIDS.”

All in all, a grim scenario, according to which testing
positive for HIV antibodies would truly be a “prognosis for
death”. I am skeptical, but as a survey research professional I
reserve the right to withhold judgment until I have seen full
reports on both San Francisco studies. At minimum such reports
would have to include full descriptions of methodology; all
questionnaires, recording forms, and field materials; sampling
procedures; and computer tabulations.

At any rate, I do not accept the proposition that Koch’s
postulates should be abandoned in favor of epidemiological
correlations. This would be a step backward, a step away from
scientific rigor, a stop towards impressionism and confusion.

Murray Gardner

Murray Gardner, Chairman of the Department of Pathology,
University of California at Davis, spoke about lentiviruses and
animals. The man is apparently a failed stand-up comedian.
During his presentation he danced back and forth behind the
table, gesturing wildly, urging the audience to laugh along with
him at the absurdity of doubting, even for a moment, that HIV was
the cause of AIDS. We were told that the animals had “little
understanding of co-factors”, that their diseases had “nothing to
do with lifestyle”, and so on.

Gardner had begun his clown act even earlier, making faces
during Rubin’s presentation. Virtually nothing Gardner said was
relevant, and little was memorable, except perhaps the mistakes.
A slide of his referred to the “pathogenicity of new HIV strains,
e.g., HIV-2”. This is wrong: HIV-1 and HIV-2 are not different
strains of each other; they are completely different viruses;
they differ in genetic structure by up to 60%; they do not have a
closely-related common ancestor.

(Based on these facts, Dr. Joseph Sonnabend, an independent
AIDS researcher in New York City, has formulated an “evolutionary
argument” against the HIV hypothesis, which runs roughly as
follows: There is no longer just one “AIDS virus”; there are
several, perhaps as many as four or five at last count. It is
now claimed that both HIV-1 and HIV-2 are capable of causing
AIDS, a disease which allegedly appeared in the world for the
first time only a few years ago. However, viruses are products
of evolution, and very ancient — there is no such thing as a
“new” virus. The proposition that, within the space of a few
years, two different viruses, each capable of causing the same
new disease, should have come into being, or should have gone
from an animal reservoir to susceptible human populations, is
seyond the bounds of probability.)

Gardner concluded his presentation by winking at the
audience. It reminded me of one critic’s comment on a cheaply
made horror movie — that the zombies were less frightening than
the attempts at humor.

Roger Detels

Roger Detels, Professor of Public Health, University of
California at Los Angeles, began his talk by saying that it was
good to continue questioning judgments. In context, this
amounted to an apology to Duesberg and Rubin for the rudeness
with which they had been treated. It was a gracious gesture on
his part.

Detels discussed the San Francisco “Multi-Center AIDS Cohort
Study”, in which an annual “attack rate” of 5% was found among
the seropositive gay men studied. That is, each year 5% of the
seropositives came down with AIDS. (Harry Rubin was to point out
later, that if 1-3 million Americans are seropositive, according
to CDC estimates, and if the annual attack rate is 5%, simple
arithmetic indicates that every year 50,000 to 150,000 people
ought to develop AIDS.)

During the question period, pathogenesis was mentioned
again, and Haseltine entered the fray, insisting that there were
plenty of mechanisms that could explain pathogenesis, and that it
was not necessary to discuss it.

Questions From The Audience

The first audience participant was Harvey Bialy, Research
Editor of “Biotechnology”. His remarks were rather technical, and
can be found in more detail in an editorial in the February issue
of “Biotechnology”. The gist is that several recent articles have
cited antigenemia findings to suggest that HIV may, after all, be
active during the fatal, late stages of AIDS. However, the
papers contain serious mathematical and other discrepancies.
Bialy maintained that it was the responsibility of scientists, as
well as journalists, to look at data critically and ask the hard
questions.

The second speaker from the audience was Coulter, who asked
whether findings from the San Francisco City Clinic study, based
on a sample of gay men who had hepatitis B, and who were highly
promiscuous and heavily into recreational drugs, could be
extrapolated to all of the people in the U.S. who were
seropositive. For some reason, the epidemiologists were either
unable or unwilling to answer his question. Coulter persisted,
asking the question in several different ways, each of which was
perfectly clear. But the “AIDS experts” could not respond. This
was truly amazing, for the question was one of the most basic in
all of statistics. It is the question of how representative a
sample is of a particular universe or population — of whether
one can project findings from the sample to the target universe.

Next, Dr. Nathaniel Lehrman, an independent researcher from
Long Island, spoke, emphasizing the need to re-examine the
etiology of AIDS, not only because of the questions raised by
Duesberg and others, but because its epidemiology is far more
consistent with a toxic illness than with an infectious one. How
could AIDS be only an infection, and spreading so rapidly, when,
according to Surgeon General C. Everett Koop, M.D., not one of
750 accidental inoculees with the blood or body fluids of known
AIDS patients developed the disease, and only three then
developed antibodies to HIV?

Chemical causes of immune deficiency, stated Lehrman, have
long been known, and one group of chemicals, known to produce
immune suppression, may be a cause of AIDS in the homosexual
community: inhaled nitrites, or “poppers”. And although poppers
are banned by law in New York State, they are as freely available
on New York streets as any other illegal drug. Could other
chemicals also be involved in producing immune suppression and
AIDS? Lehrman concluded by saying that the possibility that
chemical toxicity plays a significant causal role in AIDS ought
to be investigated, and that therefore changes, or at least
additional methods in diagnosing, treating and researching the
syndrome should be adopted. One such step would be
spectrophotometric and similar investigation of AIDS patients for
unusual, immune-suppressive substances within their bodies.
I spoke next, and said it was high time that those who
advanced the hypothesis that HIV was the cause of AIDS should
publish a monograph in an appropriate journal, which would bring
together all the evidence supporting their hypothesis, which
would take into account the critiques made by Duesberg and
others, and which would contain proper references for all
assertions made. Then I said that the epidemiological research
on AIDS had been very poor, completely unacceptable by the
standards of professional survey research. Ever since 1984,
Public Health Service surveys have concentrated only on such
things as “modes of transmission”, or “risk factors for
seroconversion”, as a result of which we know almost nothing
about the characteristics of PWAs. We have no idea what the IV
drug users with AIDS are like, other than the “risk group” label
that has been slapped on them. Finally, I said it was
disgraceful that AZT was still being marketed, a poisonous drug
without a single scientifically-established benefit. When would
the AIDS establishment admit that the AZT trials, on which
approval of the drug was based, were fraudulent?
Finally, Specter, the reporter from the Washington Post,
demanded that Duesberg give him a yes or no answer to the
question, “Do you still maintain that someone should be overjoyed
to find out he is [HIV-antibody] positive?” Duesberg paused, and
way one does when confronted with an obstreperous barbarian,
Specter started yelling, “Answer the question! Yes or No? Why
won’t you answer the question?” When he finally got a chance,
Duesberg replied that he would answer the question, but in his
own words, not Specter’s. Duesberg repeated his position, but
the nuances of his answer were not appreciated by Specter.

Summing Up

For the debate on the cause or causes of AIDS to move
forward, a number of questions of fact must be resolved: Does HIV
kill cells in vivo (in living organisms)? If so, how?
References? Is HIV really “more complex in its genetic makeup
than any other known retrovirus” (as asserted in AmFAR’s “Review
of Operations: 1985-1986”)? References? From what percentage of
PWAs can HIV be isolated? From what percentage of PWAs can pro-
viral DNA be detected? References? What is the definition of a
“good lab”? References? Is viremia found in PWAs? If so, what
virus titers are obtained, when, how, etc.? References? Are
there (as asserted by Gallo et al.) both pathogenic and non-
pathogenic strains of HIV? If so, how do they differ?
References? Can “nude mice” really mount a vigorous immune
response (as asserted by Haseltine)? Is a full report available
on the epidemiological research conducted in San Francisco?

The forum exposed the bankruptcy of the arguments used by
the HIV advocates. Only a few weeks ago they were trotting out
at least half a dozen speculative mechanisms to explain how HIV
might cause AIDS; during the forum, such speculations were
abandoned, and the official line was, “We don’t need to explain
pathogenesis.” The “AIDS virus” crowd cannot agree on even the
most crucial questions of fact, as indicated above. At one
moment HIV is ferociously killing T-cells; the next moment, “AIDS
experts” are desperately scrounging around for “indirect
mechanisms”. “Epidemiology” has been called in as a last ditch
effort to rescue the HIV hypothesis, and yet the epidemiology
conducted by the AIDS establishment to date has been quite bad,
totally unacceptable by the standards of professional survey
research. While the San Francisco studies may “strongly support”
the HIV hypothesis, they could not prove it, even if the data
were correct (and this cannot be determined until a proper report
is issued), because there remain alternative explanations to
account for the correlation between HIV antibodies and AIDS —
namely, that HIV is itself an opportunistic infection in the AID
Syndrome, that HIV is a marker for AIDS.

I am more sure than ever that HIV is not the cause of AIDS.
If the HIV advocates were sure of their hypothesis, they would
want to enlighten us; they would want to publish their arguments
in a proper scientific journal, complete with references. They
would not need to resort to stonewalling, deception, and personal
abuse.

References

1. For Duesberg’s ideas see:
Peter H. Duesberg, “Retroviruses as Carcinogens and
Pathogens, Expectations and Reality”, Cancer Research, March 1,
1987.

— “A Challenge to the AIDS Establishment”, Bio/Technology,
November 1987.

Celia Farber, (interview with Duesberg) “a.i.d.s.: Words
From the Front”, Spin, January 1988.

John Lauritsen, “Saying No to HIV: An Interview With
Professor Peter Duesberg”, New York Native, July 6, 1987;
Christopher Street 118.

Russell Schoch, “The ‘AIDS virus’ tests negative”,
California Monthly, December 1987.

2. Michael Specter, “Panel Rebuts Biologist’s Claims on Cause of
AIDS”, Washington Post, April 10, 1988.)

3. See, for example, articles in the New York Native and the New
Scientist (February 12, 1987).

4. Celia Farber, op.cit.

5. Harvey Bialy, “Commentary: Where is the Virus? And Where is
the Press?”, Biotechnology, February 1988, p. 121.

6. See my two articles, “AZT on Trial” (Native, October 19, 1987)
and “AZT: Iatrogenic Genocide” (Native, March 28, 1988).

[Copyright John Lauritsen 1996. Only non-commercial reproduction is
permitted.]

The book, THE AIDS WAR, is a collection of John Lauritsen’s
major writings on AIDS, going back to February 1985, and can
ordered directly from him.

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