HIV Cause Of AIDS?
Peter H. Duesberg & Brian J. Ellison Respond to Their Critics
Policy Review Dec. 1990
1990 issue of "Policy Review" contained one of the three
or four most-talked-about articles in the history of the magazine.
"Is the AIDS Virus a Science Fiction?: Immunosuppressive
Behavior, Not HIV, May Be the Cause of AIDS," by Professor
Peter Duesberg of the University of California at Berkeley and
his doctoral student Bryan Ellison, put into layman's language
an argument that Duesberg, one of the world's leading retrovirus
researchers, has advanced several times in scientific publications.
The article elicited more letters to the editor than any in "Policy
Review's" history, and our offices received more comments,
both positive and negative, than on any other article in recent
to the article have been sharply critical, as one would expect for
an argument challenging the reigning paradigm of most leading scientists
and doctors closely involved with AIDS, as well as of most conservatives
who are deeply knowledgeable about the disease. But a large number
of readers said they were absolutely fascinated by the questions
Duesberg and Ellison raise about prevailing AIDS wisdom, and they
wondered why Duesberg's argument has received virtually no public
attention. Whether or not one agrees with Duesberg's and Ellison's
arguments-and the important public policy implications if they are
correct-it does seem that there has been a rush to judgement implicating
HIV as the cause of AIDS and a distressing politicization in the
scientific community that refuses even to entertain contrary views.
is a sampling of letters we received about the Duesberg-Ellison
article, together with a response from the authors.-Adam Meyerson
I was stunned
by the article by Peter H. Duesberg and Bryan J. Ellison. I felt
like I had been on Mars for 50 years and had just returned home
to find that everything I had come to know about AIDS was no longer
In the interest
of brevity, I will point out only seven statements by the authors
that are completely at variance with current knowledge:
increasingly indicates that large numbers of people infected with
HIV, probably the majority, will never develop AIDS."
it were true. Numerous cohort studies have proven otherwise. A group
of 6,000 homosexual men in San Francisco followed since 1978 has
show the following pattern of progression from infection to illness:
Among the 121 men who became infected before 1981, 52 percent had
developed AIDS by 1988-89; 22 percent had developed AIDS-related
conditions; 11 percent had generalized lymphadenopathy; and 15 percent
remained asymptomatic but were expected shortly to develop symptoms.
syndrome began to level off in 1988."
It is widely
known and accepted that the leveling off in new AIDS cases among
homosexual men in New York, Los Angeles, and San Francisco was the
direct result of therapy with AZT, an antiviral drug that slows
progression of AIDS and therefore postpones diagnosis. Cases among
infected intravenous drug users, the majority of whom could not
afford to take AZT prophylactically, have risen steadily, accounting
for 21 percent of all cases in the United States, and 47 percent
of new cases in New York City.
are no confirmed cases of AIDS among health care workers after accidental
This is simply
false. Infections and subsequent AIDS cases resulting from needle-stick
exposures are well known and documented. One physician, infected
in precisely this manner in 1985 and diagnosed with AIDS in 1988,
addressed the Sixth Annual AIDS Convention last June in San Francisco.
diseases without HIV. "
Ellison note that Kaposi's sarcoma has been diagnosed in some homosexual
men who are HIV-negative. Your authors failed to mention a hypothesis
gaining increasing support: that Kaposi's sarcoma may well be the
result of a completely separate etiologic agent from AIDS, transmitted
in homosexuals through anal intercourse, as is AIDS. Kaposi's sarcoma
occurs rarely among other HIV-infected individuals, such as blood-transfusion
recipients intravenous drug users, and hemophiliacs. This observation
is simply not a legitimate "flaw" in the HIV hypothesis.
AIDS diseases seen among infants tend to be the typical pediatric
is disgracefully inaccurate. Pneumocystis carinii pneumonia (occurring
in 40 percent of pediatric AIDS cases) is a typical childhood disease?
Lymphocytic interstitial pneumonitis? Fungal infections of the esophagus
or lungs? Cryptosoridiosis? Cryptococcal meningitis? Even before
the advent of antibiotics and vaccines these infections were never
and Harold Jaffee thoroughly trounce this assertion in their commentary
appearing in the June 21, 1990, issue of the British medical journal
"Nature", citing the etiological agents of cholera, polio,
and tuberculosis as well-known exceptions to the outdated postulates.
They go on to explain that other researchers, following modernized
versions of the postulates, have convicted HIV as the causative
agent of AIDS.
people with AIDS] the use of AZT and similar antiviral-specific
drugs should be avoided."
With this particular
statement the authors cross over the border of science into the
realm of quackery. AZT, certainly, is an imperfect drug. It is not
a cure. But as numerous studies published in reputable medical journals
establish, AZT is the best and only antiviral treatment currently
available for HIV infection. To recommend that HIV-infected persons
forgo such treatment based on "anecdotal case descriptions"
is a grievous misinterpretation of scientific evidence.
I am deeply
distressed about this article and its contents, which are, at best,
at the fringe of science.
American Council on Science and Health
In their recent
article Duesberg and Ellison argue that HIV is not the causal agent
of AIDS and that preventive measures based on this premise are "misguided."
As an epidemiologist involved in the investigation of HIV infection
and AIDS, I cannot accept these assertions. Here are some of my
1) Among 286
homosexual men who were already infected by HIV in 1984 and were
followed with twice-yearly examinations by my colleagues and me,
140 (36 percent) developed AIDS, and 80 died of AIDS in the ensuing
five years. Among 40 homosexual men infected by HIV after entering
the study, two (5 percent) developed AIDS. Among 370 homosexual
men, simultaneously recruited for study from the same source and
who remained uninfected during the five years of observation, none
2) Among the
386 men already infected by HIV in 1984, 193 (50 percent) had T-helper
cell counts below 500 per microliter of blood on initial examination,
which among the 370 uninfected men, only 18 (5 percent) had T-helper
cell counts lower than 500 per microliter. A deficiency of T-helper
cells is the key factor causing the immune deficiency, which, in
turn, is responsible for the wide spectrum of clinical manifestations
of acquired immune deficiency syndrome (AIDS).
3) In the HIV-infected
men, T-helper cell counts fell, on average, about 80 per microliter
in each year of observation. Less than 15 percent of HIV-infected
men failed to show a decline in T-helper cell counts during the
follow-up period. The average T-helper cell count in uninfected
men remained constant over the five years of observation.
4) In our study,
and in all other studies, acquisition of infection by HIV among
homosexual men was primarily associated with a particular sexual
practice, receptive anal intercourse with numerous different partners.
Acquisition of infection was not related to drug use, per se, but
was highly correlated with needle sharing during drug use. These
observations are fully consistent with an infectious mechanism of
5) The rate
of infection by HIV in the 410 initially uninfected men in our study
declined from an annual average of 6 percent for the period 1984-85
to less than 1 percent during 1989. This decline was associated
with the adoption of recommended safe sexual practices by a large
proportion of study participants.
Ellsion emphasize the failure of HIV to satisfy the criteria of
Koch's postulates. However, even when he was restating criteria
earlier proposed by his teacher, Jacob Henle, Robert Koch knew that
certain pathogenic bacteria, in particular the tubercle bacillus,
did not fully satisfy the criteria. In modern times, established
pathogens such as poliovirus do not satisfy Koch's first or third
postulate, i.e., the virus cannot be isolated from all cases and
only a small proportion of infected persons develop disease. Duesberg
and Ellison are wrong when they claim that no medical workers, accidentally
infected, have developed AIDS. Of the 27 documented cases of HIV
infections acquired through accidental infection by medical workers,
two have developed AIDS.
evidence supporting a causal role for HIV in the etiology of AIDS
is overwhelming. The modes of transmission of HIV have been established
and provide the basis for a rational approach to prevention. However,
an understanding of the pathophysiology of HIV infection remains
incomplete. As this understanding develops many of the apparent
paradoxes enumerated by Duesberg and Ellison may be resolved.
of California at Berkeley
Ellison repeat misleading and fallacious arguments that have been
refuted many times in other journals. I shall reiterate some of
were a great advance a century ago.
no longer encompass our increased knowledge of infectious disease.
Even so, the relationship of HIV to AIDS does in fact fulfill the
modern version of Koch's postulates.
statements in the Duesberg and Ellsion article, certain strains
of simian immunodeficiency virus do cause an AIDS-like disease in
monkeys; HIV is very different in genetic structure form most other
retroviruses (it has at least five additional genes); the distributions
of HIV and AIDS are similar when allowance is made for the long
latent period and for differences in reporting; there is now a drastic
decease in the proportion of pediatric AIDS attributed to transfusion
(there has been an increased in the number of cases because the
latent period after infection until appearance of clinical illness
ranging from 2 to 15 years); there are well-established instances
of health care workers with no other risk factors becoming infected
with HIV and then developing clinical AIDS, as exemplified in the
highly publicized recent New York City case; and numerous examples
of heterosexually transmitted AIDS directly linked to HIV seroconversion
without any other risk factors (or the life-style factors calmed
by Duesberg and Ellison as the cause of AIDS) have also been well
and tragically, mothers infected with HIV pass the virus to about
one-third of their offspring, although all offspring of HIV-infected
mothers received antibodies to HIV.
show a large excess of AIDS and related symptoms in HIV-infected
children of HIV-infected mothers compared with uninfected children
of HIV-infected mothers. For example, in a study by Goedert, 15
of 16 HIV-infected children of HIV-infected mothers had AIDS or
pre-AIDS symptoms, while none of 39 uninfected children of HIV-infected
mothers were ill. In total, 72 percent of the HIV-infected children
of HIV-infected mothers had the disease, compared with only 5 percent
of the uninfected children. Duesberg and Ellsion state that "the
risk behavior of many of their mothers has reached these victims."
It is clear that what reached the children was HIV.
That HIV causes
AIDS is well established. An anti-HIV therapy, AZT, has actually
decreased the rate of appearance of new cases of AIDS. However,
there are still many unanswered questions about the pathogenesis
by HIV, about how to develop a safe and effective vaccine against
HIV, about how to stop behavior that results in transmission of
HIV, as well as how to pay for treatment of HIV-induced disease,
and many others. (The majority of the federal spending on AIDS is
not spent on research, but on treatment.) The only way we will stop
the AIDS epidemic is through more biological and behavioral research.
Department of Oncology
Laboratory for Cancer Research
I was profoundly
disappointed to learn that "Policy Review" would print
anything by an individual who has been so discredited in the scientific
community as Peter Duesberg. His ideas are not only wrong, but incredibly
When we formed
our organization, Americans for a Sound AIDS/HIV Policy, over three
years ago, we researched intensively to find the truth regarding
HIV disease. We found a dramatic range of opinion on this topic,
often being biased by either pro-or anti- homosexual opinions. The
least biased studies have been done by the armed forces.
at Walter Reed
is completely thorough in its research in order to protect is personnel,
since, in time of war, its soldiers serve as its front-line blood
bank. Among other things, the military conducted extensive surveys
in Africa and other countries (many of these unpublished), as well
as screened its entire active force of over two million individuals,
of whom presently more than 6,000 are infected. It has also tested
all civilian military applicants since October 1985 for HIV virus.
The data generated by these extensive studies fully conclude that
HIV is a progressive disease that causes a slow but relentless destruction
of T-cells and eventually results in the individual succumbing to
what would be otherwise non-life-threatening diseases.
at Walter Reed Army Institute of Research found a progressive decline
in the average number of T-cells from time of HIV infection until
symptomatic AIDS and death. This finding contradicts Duesberg's
statement that "the number of T-cells lost at any time would
be roughly equivalent to the number lost from bleeding from shaving.
Such losses could be sustained indefinitely without affecting the
immune system because the body constantly produces new T-cells at
far higher rates."
assertions that "virtually no reactivation of the virus occurs
when AIDS patients develop sickness" and that "after the
body produces antibodies against HIV the virus remains at low levels
for the rest of that person's life," are equally false. As
the number of T-lymphocytes declines, the volume of virus in body
fluids increases. This is not theory or hypothesis. This is reality.
nature of the virus is further detailed by numerous studies showing
that those infected with HIV progressively worsen through the diminution
of T-cell counts. Most major clinical trials, involving therapeutic
drugs or treatments use T-cells as a prime marker for disease progression.
This is accepted scientific practice and not witchcraft as Duesberg
would have readers believe.
postulates, Duesberg is mistaken again when he writes, "until
the recent advent of highly sensitive methods no direct trace of
HIV could be found in the majority of AIDS cases." Incorrect.
Ninety-five percent of late-stage AIDS patients at Walter Reed Army
Medical Center in Washington, D. C., could be cultured and all tested
positive for HIV-at all stages. Duesberg alleges that the virus
level "is typically so low" that it could not be isolated.
Equally false. Duesberg maintains that "when accidentally injected
into health care workers, even tough the virus successfully infects
those hosts," these people didn't develop AIDS. Again, incorrect.
Two highly publicized lawsuits were settled recently by Johns Hopkins
with Dr. Anoun and New York City's Health and Hospitals Corporation
with Dr. Prego. It was acknowledged that their infections occurred
on the job and both doctors now have symptomatic AIDS. There are
biggest misrepresentation of all is the statement that "evidence
increasingly indicates that large numbers of people infected with
HIV, probably the majority, will never develop AIDS." All evidence
now show that HIV will claim all whom it infects. The epidemic continues
to increase. Annualized cases ending in June 1990 totaled 40,006
versus 33,512 cases reported through June, 1989. The epidemic will
continue to claim ever-increasing numbers and percentages of people.
The Centers for Disease Control recently reported staggering HIV-infection
rates, as high as 7.8 percent in certain neighborhoods in the Northeast.
civilian military applicant rate, it is important to note that in
the six most heavily infected counties in the country today, the
ration of young me to women infected with HIV is now one to one.
That means that ultimately the ratio of men to women with AIDS in
that age bracket will approach one to one. Recently reported cases
of AIDS-which reflect HIV infections five to 15 years ago-have no
bearing on present infections, other than to reveal that the epidemic
is becoming a heterosexual epidemic among young people. It is not
true, as Duesberg states, that, "males with HIV are more likely
than females to develop AIDS even though they have the same virus."
He also states that the proportion of men to women in reported AIDS
cases "has not changed since AIDS was first defined."
Again, untrue. The ratio, in fact, has dropped from about 13 to
1, males to females, to about 9 to 1 today. Duesberg would be interested
to know that the CDC's AIDS case definition actually does not require
a positive HIV test to qualify as AIDS. In all likelihood some individuals
in the past were define as AIDS cases and yet were not HIV-infected.
This would account for some of the long-term survivors of AIDS who
may never have had HIV disease, and were able to compact the other
opportunistic diseases effectively.
arguments about risk behavior have some validity in that this is
a disease acquired through intimate sexual or intravenous contact.
However, his statements are much more misleading since there are
those he wouldn't classify in any "risk group." Many young,
sexually active heterosexuals are now becoming infected and will
be at risk for contracting this disease in the future. In fact,
heterosexuals are now the fastest-growing group of reported AIDS
claims that AZT is nearly the only treatment prescribed to people
who are HIV-infected, while conventional diseases are neglected.
This is also blatantly untrue. Other diseases are treated. However,
because the individual no longer has a functioning immune system,
these diseases in time overwhelm the body, even with medications
to defend against them. Once again, Duesberg is utterly wrong when
he calms that "HIV is inactive by the time AZT is administered."
One of the
author's statements is correct; that his risk hypothesis should
reduce the fear of HIV infection. It certainly will do that. As
a result many will believe they aren't at risk, and will subsequently
become infected and die. Having worked with many families who are
suffering from this disease through all modes of acquisition of
this virus, we can say that his recommendation that sexual partners
of HIV-positive need not be contacted or traced is perhaps the most
irresponsible position that could be taken by anyone in this epidemic.
It is immoral
and reprehensible to leave at risk unsuspecting sexual partners,
many of them loving spouses. Duesberg's conclusion that "the
HIV hypothesis has not yet saved a single life," is totally
untrue. We personally know individuals who have been saved because
their spouse learned of their infection in time to alter behaviors.
We also know a number of children who tragically are losing both
parents because a spouse wasn't informed. These are real people
who are dying at very early ages and leaving behind fine young children
whom we will all have to take care of in some way.
Americans for a Sound AIDS/HIV
NOT A FICTION
AIDS Virus a Science Fiction?" ask Peter H. Duesberg and Bryan
J. Ellison. Had you asked some practicing physicians, or even a
mining engineer with knowledge of the situation in Africa, the answer
would be clearly "No."
sets some of its errors in large, bold-face type, e.g., "there
are still no confirmed cases of AIDS among health workers after
accidental infection with HIV." There is a multimillion dollar
lawsuit in progress about one such case. Another is described in
the first person in the September 7, 1989, issue of the "New
England Journal of Medicine."
combination of prolonged malnutrition with heavy use of alcohol,
heroin, cocaine, and antibiotics...lead to complete immune system
collapse"? We didn't see this when I was a student or intern
in inner-city hospitals. And when we see it now, the HIV test is
usually positive. (Yes, all tests known to man have false negatives.
And there is more than one cause of immunodeficiency.)
departments may be delighted to hear that "there is no need
to trace the sexual partners of HIV positives," since most
of them don't do it anyway. But the prevalence of seropositivity
for HIV in regular heterosexual partners of infected persons has
ranged from 10 percent to 60 percent in various studies.
how many Africans have died of AIDS. Some say that as few as 1 percent
of actual AIDS deaths are reported. But there are armies of orphaned
children, and workers refuse to go to some mining communities where
the prevalence of disease is especially high.
There are too
many errors in this article to cover them all.
most obvious one is the assertion that syphilis is "difficult
to test for."
M. Orient, M. D.
OF MANY IMMUNOSUPPRESSORS
of Duesberg and Ellsion's article claiming that HIV is not the cause
of AIDS that the authors are lone wolves crying in the wilderness,
let me add my voice to the growing chorus. While I am not convinced
that HIV is irrelevant to understanding AIDS-after all it is highly
correlated with the syndrome-I am not convinced that it is any more
important that other immunosuppressive agents associated with AIDS.
On the contrary, I believe existing evidence demonstrates that HIV
is neither necessary nor sufficient to cause AIDS.
linking HIV to AIDS are nowhere near as good as the public are led
to believe. Reference to the Centers for Disease Controls' own data
reveals that 5 percent of AIDS patients test for HIV never display
signs of infection, and that less than 50 percent of AIDS patients
have been tested for HIV.
of homosexual men with AIDS and without HIV infections have been
verified. In response, HIV proponents are lobbying for a change
in the definition of AIDS to exclude HIV-free cases. These people
do not, apparently, understand two things: 1) that defining AIDS
by HIV and simultaneously demonstrating that HIV causes AIDS is
a tautological, and therefore bankrupt, reasoning; and 2) that altering
the definition of AIDS does not alter the fact that HIV-free people
can and do develop the same set of opportunistic infections as those
who are HIV-infected. Whether these HIV-free cases are listed as
AIDS patients or not, there are still medical patients whose syndrome
is in need of explanation. Logically, HIV is not therefore, necessary
to cause the development of these symptoms, and other causes of
what we now call AIDS must exist.
My own research,
which was published this summer in "Perspectives in Biology
and Medicine," suggests what these other causes of acquired
immunosuppression may be. Briefly summarized, all of the following
agents have been demonstrated to be immunosuppressive prior to the
discovery and HIV, and all are highly associated with one or more
AIDS risk groups: immunological response to semen following anal
intercourse; the use of recreational drugs such as the nitrites
("poppers" and "snappers"); chronic antibiotic
use (often associated with promiscuity); opiate drugs; multiple
transfusions; anesthetics; malnutrition (whether caused by "gay
bowel syndrome," drug use, poverty or anorexia nervosa); multiple,
concurrent infections by diverse microbes; and infection by specific
viruses such as cytomegalovirus. Epstein-Barr virus, and hepatitis-B
virus (all of which are as highly associated with AIDS as is HIV).
these agents, including cytomegalovirus, hepatitis-B virus, opiate
drugs, and repeated blood transfusions, are know to caused the same
sort of T-cell abnormalities that are found in AIDS, and which are
usually attributed (perhaps inaccurately) to HIV infection. The
other agents cause a wider spectrum of immunosuppressive responses,
and probably explain why more than simply T-cells are non-functional
in AIDS patients. Every AIDS patient has several of these immunosuppressive
agents at work in his or her system in addition to, and sometimes
in the absence of, HIV. We cannot, therefore, logically conclude
that HIV is the sole or even the main cause of immunosuppression
Now, if the
so-called life-style theory of AIDS is correct, one important implication
is that AIDS should not be a new syndrome. It is not. I am one of
only a handful of scientists who have bothered to search intensively
through the back issues of medical journals for odd cases that match
the CDC surveillance definition of AIDS. So far I have found hundreds
of such cases, extending back to 1872 (the date when the first opportunist
disease associated with AIDS was identified). I have also scoured
the medical literature for data relevant to changes in the life-style
risks associated with immunosuppression. What I have found is very
Kinsey report of 1948 indicates that the average homosexual man
had a sexual encounter no more frequently than once month, by 1980,
the advent of gay bars and bath houses had increased this average
to dozens per month. Gay AIDS patients have often had thousands
of sexual partners. Medical reports of complications arising form
AIDS-associated high-risk activities such as anal intercourse and
fisting are first mentioned in the medical literature only at the
beginning of the 1970's, and become increasingly frequent thereafter.
From 1060 to 1980, the rates of syphilis triple, gonorrhea quadruple,
and diseases related to "gay bowel syndrome" quadruple.
These increases were found only among gay men, but not among heterosexual
men or women.
From 1960 to
1980, hepatitis-B cases rose 10 fold, in part due to sexual transmission
in gay men, and in part to IV drug abuse. Arrests on opiate-related
drug charges rose nearly 20-fold during the same period. There is,
then, no doubt that AIDS was preceded by medically evident changes
in life-style among those groups at highest risk for AIDS, and these
changes are such that not only HIV, but the entire spectrum of immunosuppressive
agents mentioned above became increasingly prevalent in these groups.
indicate to me that HIV is not sufficient to explain the manifestation
of AIDS or its recent appearance. Many other factors are also at
work. It is a tremendous mistake to base our policy decisions concerning
AIDS on an exclusive HIV basis. Far from undermining current drug
prevention and safe sex programs, the recognition of non-HIV immunosuppressive
factors in AIDS suggests that these programs are failing because
they are too narrow. AIDS will only be understood when we begin
to explore the ways in which anal sex, infections, drugs, blood
products, anesthetics, antibiotics, and malnutrition interact. At
present, we know almost nothing about such interactions. Since increasing
evidence from the laboratories of the discoverer of HIV indicates
that HIV needs immunosuppressive co-factors to be active, such studies
are clearly needed. In the meantime, those who wish to avoid contracting
AIDS should avoid all potential causes of immunosuppression, not
just HIV. And those who are HIV-positive but not ill may find that
if they, too, avoid this lengthy list of immunosuppressive co-factors,
they too will stay healthy.
Professor of Physiology
expressed for some years in TV programs, magazine articles, and
my book "AIDS: The HIV Myth," has been the subjective
element in scientific research. Medical science in particular is
presented to the public as a seamless body of unchallengeable knowledge,
when fact it is a complex mass of conflicting beliefs, each supported
by a foundation of fact, but buttressed by the vested interest of
research institutes and fashionable theories.
This has never
been more true than in the case of the HIV theory. But there is
another element here. There is something about the heady mix of
science and sex in this theory that inspires extremes of intolerance
in those who espouse it. Anyone questioning the link between HIV
and AIDS is met with an unreasoning fury or an offended refusal
to discuss the matter. The hysteria directed against critics of
the HIV theory suggests that it is not a matter of scientific fact
that is being defended here but a belief system.
This is particularly
disconcerting because of the very poor quality of scientific thinking
behind the HIV theory. To give some examples: Current scientific
method says that to prove a theory we should actively seek information
that would disprove it. It is by resisting these repeated challenges
that the theory becomes stronger or, instead, it fails and gives
way to another theory more appropriate to the evidence. In fact,
since HIV was declared the cause of AIDS at a press conference in
April 1984 (before the scientific papers that were supposed to support
it were even published), there have been no experiments to test
the HIV theory.
All the work
in this multimillion dollar research project has been designed and
carried out to support the HIV theory of the cause of AIDS.
One of the
pillars of scientific thinking is predictive testing. As a part
of policy-making, government scientists make predictions of the
number of AIDS cases based on the current HIV infection rates. The
predictions have turned out to be wrong by orders of magnitude.
There are far fewer AIDS cases that would be predicted by the number
of HIV cases. Under the rules, if your prediction doesn't come true,
you re-examine the theory. What the HIV supporters do in these circumstances
is to conjecture that maybe their assessment of the number of people
with HIV infection was wrong or maybe the incubation period is longer
than they thought. The parameters of the predictive experiment have
to be adjusted in retrospect to fit an unwelcome outcome. The only
thing they will not do is re-examine the theory that HIV alone and
of itself causes AIDS.
The use of
mainly anecdotal "evidence" from Africa in defense of
the HIV theory is particularly shocking. In 1988 and 1989 the AIDs
epidemics failed to follow predictions and AIDS cases in the U.
S. and Europe began to plateau without substantially exceeding the
limits of the so-called at-risk population. What should have happened
was a wholesale re-evaluation of the HIV theory. Instead, its supporters
told us to look to Africa, which would demonstrate they had been
right all along. So the two continents with the greatest capacity
for collecting medical information and analyzing statistics about
the epidemic were relying for confirming avoidance not on their
own well-funded institutions, but on information garnered from the
continent with the least sophisticated health and statistical services.
The poor quality
of scientific thinking leads to shabby behavior in the conference
halls and journals. A theory that is poorly grounded has to defend
itself form it critics on the basis of sneer and insult, for it
has no honorable weapons of debate.
failed to rise to the challenge to their theory by scientists such
as Duesberg in the scientific papers, defenders of the HIV theory
complain that criticisms of it has been made available to the public.
This will, we are told, undermine confidence in public health measures
designed to protect the general population.
I happen to
feel that the use of clean needles and condoms is a valuable public
health measure in itself without the bogeyman of HIV. But what really
interests me is the way critics of HIV theory are told to keep their
doubts to themselves because if they don't, the very theory about
which there is serious doubt might lose its influence with the public.
Thus doubt is placed in the service of certainty in the public interest.
expert advice must be evaluated by the people who are not experts-politicians,
journalists, and the public. This is part of democratic life and
a scientist has no more right to exclusion from public scrutiny
than a treasury official. All expert advice affecting our lives
must be subject to abrasive doubt. In the field of the HIV theory
this doubt has had to stifle to thrive in the scientific community.
It needs an infusion of energy from outsiders whose only interest
is to ensure that hard questions are asked and the "AIDS establishment"
is pinned down to answer them.
IN RISK BEHAVIOR
Ellison present as thorough and balanced a review of AIDS as I have
seen in print. It certainly makes a strong case for the thesis that
immunosuppressive risk behavior is at least as likely as HIV to
cause this complex array of diseases. I have witnessed the abuse
to which Duesberg has been subject for arguing this thesis. The
"coup de grace" that is supposed to silence him is that
AIDS cases among hemophiliacs and children of HIV-positive mothers
do not exhibit the risk behavior. But the article deals effectively
with those objections by showing that they, in their own way, constitute
suggestion that controlled studies be done on HIV-positive and negative
groups with equivalent risk behavior is an eminently sensible one
and I am amazed that this has not been done. This, of course, must
be done using non-HIV controls undergoing "equivalent risk
behavior" as the HIV carriers, i.e., equivalent number of anal-receptive
drug-using sexual encounters or frequency of drug use. To the best
of my knowledge, such a study has not been done, much less published.
If the authors
are correct, and HIV is essentially a reporter for high-risk behavior,
it would be difficult indeed to find the right controls. Until it
is done in a scientifically sound way, I am not willing to accept-or
to completely reject -- a central role for the virus in the etiology
of the disease. But, since such a strong case can be made for the
role of drugs, antibiotics, and related risk behavior in the origin
of AIDS, it makes little sense to recommend clean needles and condoms
while ignoring the behavior itself.
The one solid
epidemiological fact we seem to have is that the disease in the
U. S. is restricted almost entirely to certain risk groups. Regardless
of the involvement of the virus, the only sure cure is to modify
of Cell and Developmental Biology
to the Virus Laboratory
of California at Berkeley
In the spirit
of "the openness" of science we salute Peter Duesberg
for his challenging and courageous voice speaking out against the
present scientific establishment. His extensive experience and knowledge
about retroviruses lends merit to his critical evaluation of the
possible causative role of HIV in the AIDS disease.
is a fundamental difference between our judgement of the AIDS disease
and that of Duesberg. We believe that the disease of AIDS is an
infectious process. Despite our respect for Duesberg's expertise
in retroviruses, we think his assessment that no microbe, including
any mycoplasma, could possibly cause the full set of AIDS diseases
is premature. It has been know for many years that microbes known
as mycoplasmas can cause immune suppression, weight loss, diarrhea,
and chronic debilitation in animals; but mycoplasmas were not considered
fatal in humans. The recent discovery that previously unrecognized
pathogenic mycoplasma, M. incognitus, causes fatal system infections
in experimental monkeys, has suggested that this microbe could be
playing a disease-promoting role for AIDS. It is significant that
mycoplasmal infection has been found in diseased brains, livers,
and spleens of AIDS patients, as well as some HIV-negative patients
displaying similar symptoms.
the French discovered of HIV, is the most famous but not the only
eminent scientists who endorses the possibility that mycoplasmal
agents could play a significant role in AIDS. Many mycoplasmologists
worldwide have now joined the search of these microbes in patients
with AIDS. We also applaud Montagnier's courageous strong stand
at the recent International Conference on AIDS that mycoplasma could
be the key co-factor of AIDS disease.
There are many
intriguing, but certainly not well understood, biological characteristics
of M. incognitus and the infection it produces. The infection suppresses
the immune system, causes immune derangement, and can be associated
with chronic debilitating disease.
and nature of these mycoplasmas need to be carefully researched,
using modern technology. The rapidness of advances in understanding
the significance of mycoplasmal disease in humans will be directly
proportional to the amount of funds available. At present, only
a very small amount of money supports mycoplasma studies.
the most healthy and responsible scientific attitude in dealing
with AIDS research is to explore all possible avenues. To make any
conclusion lightly or prematurely, such as ruling out any possible
role of microbes in AIDS, or to commit oneself exclusively to a
particular agent and completely rule out any other possible role
of a different microbe, may all result in a greater loss of AIDS
Division of Geographic Pathology
Douglas J. Wear, MC USA
of Infectious and Parasitic Disease Pathology
Forces Institute of pathology
While we agree
with many of Duesberg and Ellison's criticism of AIDS research,
they are ignoring research (i.e., on AIDS contracted by the wives
of hemophiliacs) that appears to support the HIV hypothesis.
In our experience,
Duesberg and Ellison are overly simplistic in believing that abstinence
from risk behaviors will avert the devastation of AIDS or that the
risk-behavior theory can explain the presence of AIDS in those who
have not engaged in these behaviors.
and 1985, our group at the Institute for Thermobaric Studies worked
with over 400 individuals with AIDS, or AIDS-related complexes (ARC),
or who were at risk due to contact with AIDS patients. As did Duesberg
and Ellsion, we saw major causes of immune suppression in the behaviors
and life-styles that would make for classical (not HIV-related)
acquired immune deficiency syndrome. Included in the classical causes
of immune suppression were chronic inflammatory diseases (venereal
diseases, hepatitis, allergies, chronic irritation, infection, or
injury), chemical suppression (from any anti-inflammatory, antibiotic,
or depressant drug as well as the wide range of street drugs), and
malnourishment (including bulminia, anorexia, and laxative abuse).
time, we taught over 200 AIDS, ARC, and at-risk clients to support
optimum immune competence and minimize their exposures to immune-suppressive
drugs and behaviors.
and Ellsion hypothesize, we did see a significant improvement in
the general health of our clients, but not with everyone and not
uniformly. Initially, we attributed this to different health stabs
and varying degrees of dedication, discipline, or economic resources.
Daily documentation was made of diet, stress, exercise, sleep, medications,
and drug use. Despite the best efforts and the highest quality of
care, men continued to sicken and die, although more slowly that
those not engaged in our program.
By 1984, we
saw the resurgence of the opportunistic infections regardless of
the quality of care and decided to take a closer look at these infections
in the period prior to the antibiotic/drug era that began in 1945.
We quickly found that everything we were seeing in AIDS had been
seen before, most often and most profoundly in individuals who had
an underlying, progressing infection of syphilis.
By 1985, the
narrow focus of AIDS research and the shifting of funds out of sexually
transmitted disease areas into HIV research had severely restricted
any open inquiry into factors related to AIDS that did not directly
promote the HIV hypothesis. We were seeing research by mandate and
epidemiology by fiat. To continue our investigation, we developed
BASIS, Biological Assessment of Syphilis and Immune Suppression.
BASIS has been screening educated, affluent, health-conscious consumers
who are not engaged in risk behaviors although they may have in
the past. We continue to find a major correlation between a prior
history of syphilis and the development of AIDS independent of the
sensationalized behavior or blood transfusions, and independent
of whether they tested HIV-positive.
and Ellison, we believe that the fundamental science to prove the
HIV hypothesis has not been done. We do not, however, assert that
there is no correlation between HIV and the disease syndrome we
are seeing in AIDS. Long-term infections of syphilis, while causing
immune suppression, also foster overgrowth of viruses, odd forms
of virus, as well as other opportunistic infections. HIV may actually
be a marker for an otherwise undetected, altered form of syphilis.
We suspect it may be the "black syphilis" of Asian origin.
and Ellsion, we see the use of AZT as a political and economic solution
without real medical benefit to the patients. AZT is a know immune
suppressant that essentially shuts down the immune system. By administering
AZT to AIDs and ARC patients, few symptoms emerge that require medical
care or hospitalization until the final stage of massive system
failure from multiple infections. With AZT, the insurance companies
avoid the $150,000-$250,000 expenses of earlier AIDS cases where
9 to 18 months of hospital and medical care were threatening to
bankrupt the companies. Hospital and health care administrators,
including Medicaid officials, who saw their ruin looming were relived
that their financial exposure could be limited to a few weeks or
months by AZT administration to patients. Politicians who were reluctant
to expend more money and public resources for the care of economically
and politically disenfranchised minorities could assuage concerned
families and friends and the media that everything was being done
that could be done medically with AZT. They promised to make AZt
easier to obtain and require that all physicians see AIDS patients
urge them to go on the drug. AZT does not stop the progression of
the disease. It does not stop patients from dying. But the dying
is quiet, convenient, and cheap at $5,000 to $15,000 per patient.
that AIDS is the tip of an iceberg of immune-suppressive disorders
in our country, which if combined with syphilis could lead to a
major human die-off by the end of the century. Duesberg and Ellison
do us all a disservice by continue to promote the idea that normal
people, with normal sexual patters, who do not abuse drugs, are
not at risk.
THE HIV MONOPOLY
We agree with
Duesberg and Ellsion that the foundation of our national AIDS policy
is crumbling due to its own errors and incompleteness, and feel
that the whole thrust of HIV testing and research must be reconsidered.
in working with people with AIDS and those at risk clearly supports
a multifactorial policy.
consideration is that tens of thousands of HIV-positive people are
walking around with the fearful misunderstanding that it's only
a matter of time before they necessarily become ill and die. Many
of these pele feel sick solely because of this belief. Thus, the
possibility that HIV is not the cause of AIDS brings up issues of
psychological murder, as well as scientific error.
It is not in
our best interest to allow the HIV/AIDS establishment to maintain
their monopoly on the prevention and treatment of AIDS and it is
long past time for us to insist on open-minded, first-rate science,
rather than simply accepting the unproven assumption that HIV causes
AIDS, let alone that AZT extends life.
We hope that
medical doctors and the Food and Drug Administration will be help
accountable for the distribution of AZT based on the poor quality
of research provided in the studies, and the well- known dangers
in using this toxic and immune-suppressive drug, all to destroy
a virus of questionable pathogenicity.
of AIDS in Africa is consistent with the bold thesis of Peter Duesberg
and Bryan Ellsion that AIDS is not primarily caused by HIV, but
it contradicts the authors' suggestion that the disease is caused
simply by behavior. Their statement that "AIDS in Africa is
evenly distributed between males and females" is quite wrong;
for the majority of the 53 African countries there is a "female
preponderance of AIDS", as first noted by Dr. Neeguaye and
colleagues from Ghana. Sex parity of AIDS incidence is true only
of seven countries in East/Central Africa, and of one in West Africa
where AIDS is in the propagation phase. For the remaining 39 sub-Saharan
African countries in the introduction phase, AIDS was, until very
recently, known as a female disease resulting form international
It is well
documented that African men who use only village prostitutes are
less likely to get AIDS than town prostitute users, who are less
likely to get AIDS than city prostitute users. There must be "something"
that the city international prostitute transmits to produce AIDS.
In Arabic North Africa, for example, international prostitution
is practiced on pain of death and there is no AIDS problem. The
Duesberg and Ellsion hypothesis does not address this.
of the international connection to AIDS is from my own Krobo tribe
in Ghana, where promiscuous men who have not left the tribe do not
get AIDS. The only Krobo men-three in all-who have AIDS have been
the international prostitutes' pimp-husbands who accompanied their
repatriated wives home from the Ivory Coast. "Something"
must have been transmitted from the prostitute wives to their non-promiscuous
husbands that was not transmitted by the non-prostitute wives to
their Krobo husbands who stayed at home. How then can AIDS be said
to be non-infectious? And why do children born to Krobo families
at home, both polygamous and non-polygamous, escape AIDS while those
of families involved in the sex trade do not?
Ellsion are correct in saying that immunosuppressive behavior is
a factor in AIDS, but alone it is not enough to produce AIDS. For
example, the international prostitutes who repatriated from the
Ivory Coast to die form the bulk of Ghana AIDS patients. Many of
these repatriated prostitutes are in the third generation of their
profession. Duesberg and Ellison's hypothesis cannot explain why
these prostitutes' second and first-generation relatives never got
from Africa refutes Duesberg and Ellison's risk hypothesis. I discovered
two pockets of traditional male-male sex practitioners-one among
the Swahili Arabs and the other among some West Africans influenced
by an immigrant culture. While there is no AIDS among these rural
folk, AIDS has developed a third group of "homosexuals"-young
men who roam international hotels in Africa's largest cities practicing
the same "immunosuppressive behavior" for foreign exchange/
"Something" must have been transmitted to this last group
who were anything but malnourished.
the international link and that certain "something" in
spreading AIDS, another possible factor is that a traumatic experience
may hasten the onset of AIDS. Professor Quartey and I have established
that virgins in Africa develop AIDS within 10 to 12 weeks after
exposure. It seems that perineal trauma allows "something"
to be trams,transmitted, as happened with the 12-year old girl who
developed AIDS quickly after being raped by Ugandan rebel troops.
Similarly, HIV-positive Ugandan patients with no symptoms whatever
were suddenly tipped into AIDS by surgery, pregnancy, or even gynecological
investigations, proving that HIV alone was not enough to produce
Ellison's case against HIV is bolstered by the many cases that defy
the HIV-only theory. In Rwanda, for example, I learned of the case
of an international prostitute who gave birth to twins. The seronegative
baby died from AIDS, while the seropositive one lived. Similarly,
a seropositive Ghanian child is still alive and well without symptoms
four years after her mother died of AIDS. Duesberg and Ellison are
also correct in pointing out that malnutrition is not immunosuppressive,
but can also be present with features exactly like AIDS.
such findings, much evidence contradicts Duesberg and Ellison's
hypothesis. Studies show that in the early propagation- phase of
AIDS in East and Central African countries, the failure to screen
blood for transfusions has led to AIDS. Similarly, in the West African
countries of Nigeria and Ghana, where the HIV antibody rate in blood
donors is very low, AIDS infection through blood transfusion is
rare. The Duesberg and Ellison hypothesis fails to explain these
discrepancies. Clearly, the debate over AIDS is not over.
The best support
for Duesberg and Ellison's hypothesis comes from the success of
both tribal and non-tribal therapeutics in Africa. Traditional healers
in Africa have been tackling AIDS with varying degrees of success.
Two food items that were also found anecdotally to be therapeutic
interested me most. Papaw seeds (Carica papaya), traditionally used
in the Gold Coast (Ghana) for intestinal parasites, abdominal pain,
and diarrhea but with no know anti-retroviral action, have been
tried in Ghana in AIDS diarrhea with some encouraging results; and
the winged bean (Psophocarpuis tetragonolobus), also with no known
anti-retroviral action, has helped Ashanti women with AIDS.
treatment for AIDS is the special formulation of human alpha interferon
(KERMON) that was produced through the international cooperation
experts from Kenya, the U. S., and Japan.
It holds the
best promise for AIDS treatment and owes its efficacy less to an
anti-retroviral (HIV) effect than to an immune-enhancing capability.
Indeed, drugs with specific antiretroviral properties are less effective
in treating AIDS.
there are "pluses" and "minuses" in the Duesberg
and Ellison hypothesis. There is still a lot of rethinking to be
done regarding HIV and its relationship with AIDS, and Professor
Duesberg has been right to insist over the past four years that
the debate should not be closed.
Konotey-Ahulu, M. D.
EVIDENCE FOR HIV
There are amy
perplexing questions regarding HIV and AIDS.
may help understand the process. If many of the points Duesberg
and Ellison make are evaluated in the context of the reality of
patient care, many of the questions they pose can be answered.
patient, for example, has HIV disease for 10 to 15 years. At each
cross-section of time, as Duesberg and Ellison highlight, only a
small percentage of T-cells are found to be infected. But, these
few cells appear to die earlier than expected, so over time, gradually
fewer total cells are left. However, a few of those have received
as their legacy HIV infection to slowly continue the T-cell-depleting
effects of the disease. The fact that only a few T-cells are affect
at any one time does not change the fact that ultimately, left untreated,
HIV destroys the immune system.
On that natural
disease course, one should superimpose an individual's characteristics.
For example, it is true that one's immune system can be markedly
depressed by the use of "recreational" drugs. Substantial
percentages of the earliest cases of AIDS were in drug users, as
Terry Krieger and I pointed out in a Wall Street Journal article
as early as 1985. Drug users appear to have been the earliest patients
because they may have had a shorter HIV disease course that the
average HIV patient due to drug-induced immune system dysfunction.
It is evident
to clinicians that stopping substance abuse, during any disease,
increases a patients survival time, but that should not be equated
with a cure of the disease. Nor should immune-system dysfunction
from drug usage be equated with immune-system depression from a
diseases can produce the same objective findings. Cases of pneumocystis
and Kaposi's sarcoma occur, for example, in those who are immune-suppressed
from other factors than HIV, for example, from the effects of organ
transplants. But the clinical history is so different that it makes
good medical sense to distinguish such patients separately from
those with HIV-antibody positivity and T-cell disease due to HIV.
primary HIV medicine, unfortunately is not the ideal. It does not
always control HIV as measured by the P-24 antigen test and does
not always cause T-cells to increase as much as desired. But it
does achieve these things in statistically significant numbers,
and without AZT many people would have died much earlier. Any clinician
involved with AIDS treatment has a "control group" of
patients that for one or another reason have refused AZT. In one
of our groups we reviewed 102 HIV P-24 antigen-positive patients,
77 of who received AZT. There were 25 who did not receive AZT. These
had a 36 percent death rate, contrasted to the 77 who received AZT,
who had an 18 percent death rate.
AZT as a treatment
for HIV disease is, of course, "dangerous," like any chemotherapy
or some antibiotics.HOwever, use by patients under appropriate physician
monitoring, with continuous laboratory testing, markedly decreased
the dangers. In fact, under such circumstances, there are only minimal
side-effects from AZT evident to the patient. Further, anemia, the
most significant hazard, quite often can be controlled and revered
by concomitant use of erythropoietin, indicating, in 1990, that
AZT is not as "dangerous" as originally thought in the
mid-1980's when it was introduced.
A. Caceres, M. D.
reaction to anyone challenging the AIDS industry in any way is favorable,
but in the case of Peter Duesberg and his co-author Bryan Ellison,
I really must demur.
state that HIV does not satisfy Koch's postulate that the germ must
cause the sickness when injected into healthy hosts, because "HIV
has not been shown to cause disease when injected experimentally
into chimpanzees, nor when accidentally injected into human health
care workers." In fact, HIV does cause disease in chimpanzees,
but not AIDS. Rather, it causes a swelling of the lymph nodes, which
is one of the earliest symptoms of human HIV infection. It is startling
that the authors do not point out that pathogen-caused disease is
to a great extent animal specific. The vaccinia virus, for example,
causes the disease cowpox in cattle but does not cause the disease
in humans. Indeed, in humans it is used as a vaccination to prevent
smallpox. Further, there have been cases of health care workers
becoming infected with HIV and then developing AIDS, including the
case of a New York physician that recently made national news after
she sued the hospital. Another doctor with whom I appeared on TV
had been infected on the job and was suffering from the early stages
of the disease.
Ellison state that HIV does not satisfy another of Koch's postulates
that the germ must be found in the affected tissues in all cases
of the disease. By this standard few if any viruses could be considered
the cause of any disease since viruses are notoriously difficult
to isolate directly. (Koch, incidentally, developed his postulates
before the discovery of viruses.) This is why the use of antibodies
as viral markers was an accepted practice long before AIDS came
along. The authors shoot themselves in the foot when the point out
that "no HIV at all can be isolated from alt least 10 to 20
percent of AIDS patients; until the advent of highly sensitive methods,
no direct trace of HIV could be found in the majority of cases."
Exactly. It wasn't that the viruses wasn't there; it's that current
technology could not detect it then, and improved technology cannot
always detect it now.
are correct that the African epidemic has been exaggerated, as indeed
has the epidemic everywhere. But they incorrectly accept on its
face the estimate of Ugandan HIV-positive (800,000) and the estimate
of AIDS cases there (41,000) to assert: How could so much HIV cause
so little AIDS? The number of estimated infections is so high because
the political body that came up with it grossly exaggerated it,
but it's much more difficult to exaggerate case numbers. Why do
the authors go to Africa where the numbers are so foggy when they
can look at exact studies right at home? Two different studies of
homosexual males in San Francisco have found that after an average
of 10 years of infection with HIV, about 80 percent of the subjects
have developed full-blown AIDs or symptoms demonstrated to be precursors
to developing AIDS. A British study presented at the International
AIDS Conference in San Francisco found 23 percent of hemophiliacs
had HIV and 69 percent of those were symptomatic after only an average
of five-and-half-years' infection. One study of 172 children, which
appeared in the December 28,1989 "New England Journal of Medicine"
found that 12 percent had full-blown AIDS but all had symptoms associated
with HIV infection, indicating they were on their way to AIDS. This
is an extremely high correlation between infection and disease,
far higher than the correlation between disease and cytomegalovirus
(CMV), or poliovirus, or the bacteria that cause tuberculosis, "Mycobacterium
tuberculosis." But nobody argues that since neither CMV nor
the tuberculosis bacterium always cause disease they are not responsible
for those diseases occurring.
make some nice points, but they are points that don't prove their
case. Yes, co-factors do appear to play a role in developing AIDS,
especially in developing Kaposi's sarcoma. But co-factors also play
a role in determining whether cytomegalovirus or tuberculosis bacterium
lead to disease.
Yes, the value
of AZT is unknown because standard testing protocol was not followed.
Indeed, the worth of AZT has been grossly overstated by an AIDS
industry desperate to show results from the massive infusion of
money it has received-and taken from other disease research areas.
But again, this does nothing to disprove the HIV hypothesis.
line is that there is as much or more evidence for HIV causing AIDS
as there is for numerous other pathogens to cause the diseases we've
associated with them. Epidemiology reveals that those infected with
HIV are getting it from the blood and semen of other HIV-infected
persons. Those infected with HIV can look to cohorts of homosexuals,
hemophiliacs, and transfusion recipients and assume that changes
are they will get sick and die from opportunistic infections. Further-and
this is what is most troublesome about the authors' hypothesis-
they must assume themselves capable of infecting and ultimately
killing others. If the authors convince them otherwise, they are
doing a great disservice. What I would suggest, in perfect seriousness,
is that before the author write another article suggesting that
it is perfectly okay for HIV-infected person to have unprotected
with sex with uninfected persons or vice-versa, that they, in a
public forum, inject themselves with HIV. Apparently Duesberg has
hinted he may do it; I think he should go beyond that. Readers have
a right to know just how much faith the authors have in their own
"The Myth of Heterosexual AIDS"
H. DUESBERG AND BRYAN J. ELLISON RESPOND:
We are gratified
to find our challenge against the virus-AIDS hypothesis finally
generating the debate that should have occurred within science,
and among the tax-paying public, years ago. While our view, particularly
the risk-AIDS hypothesis is currently a minority view among scientists,
co-factors in AIDS are being viewed as important by an increasing
number of researchers; even Luc Montagnier, the discoverer of HIV,
has officially joined this modified view of AIDS. And since billions
of tax dollars have failed to save even a single life from AIDS,
the HIV hypothesis deserves review. Simply put, there is not proven
precedent for the following claims regarding HIV:
1) No virus
has ever been scientifically show to cause its disease only after
being neutralized by antibodies.
2) No virus
has ever been proven to cause disease typically after long latent
periods, rather than when it first infects a new host.
3) No virus
has ever been shown to kill thousand of times more cells than it
4) No retrovirus,
including HIV, has ever been demonstrated to kill systematically
"any" of the cells it infects.
5) No virus
has ever been found that causes radically different diseases in
different hosts (AIDS includes disease not caused by immune suppression).
6) No sexually
transmitted disease has ever remained so rigidly confined to specific
risk groups, and to males, for 10 full years.
In short, if
the HIV-AIDS hypothesis were true, it would be a truly revolutionary
break with all previous scientific experience.
categories of arguments are frequently marshalled in defense of
the virus-AIDS hypothesis:
From the field
of epidemiology, "prospective" or "longitudinal"
cohort studies are often cited in which HIV-positive patients are
followed as they progress to AIDS, while the HIV-negative control
group generally does not develop fatal disease. These studies can
be confusing to those unaware that their purpose is not to determine
whether HIV causes AIDS, but rather to find clinical symptoms that
can define various stages of sickness. The HIV-negative group is
usually selected from people in good health, who are then compared
with the HIV-positive patients with the health risks that we believe
to cause AIDS. One could just as easily conduct a cohort study,
comparing HIV-negatives with health risk to HIV-positive without
them, and get precisely the opposite results!
studies, on the other hand, would compare two groups of people,
one with HIV and the other without. The sizes of both groups should
be large, at least in the hundreds, so that occasional unexplainable
anecdotal cases of AIDS disease would be averaged out between the
groups. The two groups would be matched for every health risk that
might possibly in involved in the various AIDS diseases. Both groups
would have the same number of hemophiliacs, of the same ages, with
the same degrees of hemophilia; the same number of drug addicts
would be in both, and the groups would be matched for types, amounts,
and history of drug use; both groups would have the same number
of transfusion recipients, with the same conditions requiring transfusions;
and so on. If the HIV-positive group in such a study had significantly
more diseases than the negative group, HIV would be shown to play
a role in causing AIDS. The type of cohort studies cited by Whelan,
Winkelstein, Tmen, and Fumento is in no way this sort of controlled
study. Further, we wonder how Winkelstein could construct a study
able to determine that "Acquisitions of [HIV] infection was
not related to drug use, per se, but was highly correlated with
needle sharing during drug use."
cohort study is also used to argue that the majority of HIV-positives
eventually develop AIDS. One of the most frequently cited is the
San Francisco hepatitis-B cohort, originally selected because they
were already sick with hepatitis. The disease and death rates of
these extremely unhealthy people were projected onto the rest of
the HIV-infected populations, leading to the grossly high estimate
of future AIDS rates. But since on 13 percent of the estimated one
million American HIV-positives have actually developed anything
called AIDS over the last decade, there is no reason to believe
that such cohorts in any way reflect the condition of most HIV-positives.
One should expect death rates to be relatively high in health risk
groups like this. Again, a controlled study is needed, not careless
with biased selection methods have created the unjustified impression
that AZT has extended lifespans, but no properly conducted studies
have yet been published showing longer life resulting from this
invariably toxic drug. Indeed, recent data shows that long-time
AZT users have an incredible 50 percent rate of lymphoma, a cancer
of the white blood cells. This AZT effect is officially being blamed
on HIV, since several lymphomas are listed as AIDS diseases, although
the percentage of AIDS victims overall who develop lymphomas is
much lower than 50 percent.
diseases that do occur in the HIV-negative group of such studies
are not diagnosed as AIDS, since this syndrome is defined by the
present of indicator diseases if the patient has antibodies against
HIV; tuberculosis found in the HIV-negative group is simply called
tuberculosis, not AIDS. This presumptuous and misleading definition
of AIDS continually generated confusion among those who do not realize
that AIDS is merely a new name for old diseases.
of AIDS patients seem to be most powerful in convincing people that
HIV is a dangerous virus, despite the scientific worthlessness of
such individual situations. For such conditions as immune suppression,
individual cases can always be found in which no underlying cause
is obvious to the examining physician. In past decades, such diseases
as Pneumocystic carinii pneumonia and Kaposi's sarcoma have been
diagnosed in individuals without visible health risks. Diseases
without obvious underlying causes are typically referred to as "primary"
causes of the condition, and do not in any way indicate that something
profoundly new causes it. About 3 percent of AIDS cases cannot be
connected to confirmed health risks, which is not surprising; to
determine scientifically whether HIV causes AIDS, a controlled study
using large sample sizes is required, specifically designed to average
out such anecdotal cases (as described above).
occasional AIDS cases among babies, heterosexuals not using IV drugs,
or health care workers with HIV, defenders of the HIV hypothesis
are generally assuming, rather than absolutely confirming, the absence
of other health risk factors in each of these uncommon cases. This
is particularly true of drug abuse, which can be quite difficult
has also convinced people that wives of hemophiliacs or transfusion
recipients, presumably, having no more health risks than the general
population, often contract AIDS from their spouses. But among the
thousands of wives of HIV- positive hemophiliacs in the U. S., a
fair number are likely to contract the virus eventually. Since AIDS
is merely, by definition, a list of old diseases that are renamed
when in the presence of antibodies against HIV, one should not be
surprised to find an occasional such wife who happens to contract
HIV and, coincidentally, one of the many diseases on the AIDS list.
If a controlled study were done, comparing HIV-positive wives to
HIV-negative ones, we are confident that two groups would develop
diseases at the same rates. Playing up the few anecdotal cases of
such wives is at best irresponsible, since there is no data to suggest
they are more likely to become sick with HIV than without.
a needlestick AIDS case described in "The New England Journal
of Medicine." But that article does not confirm that the doctor
developed AIDS diseases with no health risks other than HIV; except
for slight weight loss (10 pounds) and a "bit" of fatigue,
the article fails to specify the doctor's AIDS complications. Whether
the doctor is also using the toxic drug AZT is not stated. We therefore
continue our relentless search for confirmed cases of AIDS resulting
from needlestick injuries.
the bankruptcy of the virus-AIDS hypothesis better than the claims
of Temin, Winkelstein, Whelan, Orient, Smith and Fumento that one,
or possibly two, health care workers may have contracted AIDS from
hypodermic needles contaminated with materials from AIDS patients.
The U. S. employs some five million health care workers, treating
a cumulative total of over 100,000 AIDS patients for almost 10 years;
thousand of American scientists also work on HIV. None of these
are vaccinated against HIV. Compare the one or two debatable needlestick
cases with the consequences if the nations health workers were instead
exposed for so long to polio or hepatitis virus, also with vaccination!
One of most
mistaken impressions of HIV holds that it is in some way an unusual
virus. Often statements are made about its genetic complexity and
"additional genes." Retroviruses have between 5,000 and
10,000 letters, or "bases," of genetic information; HIV
has nine thousand, a typically small number. And virtually any genetic
sequence contains some overlapping pieces of information, the "additional
genes" referred to by Temin, which can also be found in any
retrovirus. In the test tube, HIV behaves no differently from other
retroviruses in any observable way. In short, we would like to know
where this unusual complexity of HIV is hiding.
HIV would certainly
have to be an extremely unusual virus to be able to kill billions
of T-cells, though little or no active virus can be found in the
body (contrary to Smith's assertion, for which both sides of the
virus-AIDs debate would certainly appreciate a published reference).
This fatal blow to the HIV hypothesis sometimes prompts strange
and creative explanations. Cacerea, for example, believes that the
body's T-cells could be depleted if infected cells died sooner.
But the time it would take infected cells to die would not matter.
In "all" viral diseases, the virus must reproduce faster
than the host's cells if it is to overtake and deplete them. HIV
never even comes close. Further, HIV does not kill infected cells:
Robert Gallo has patented the HIV antibody testing procedure from
virus that is produced in cell lines that grow continuously, rather
than die, and Luc Montagnier has recently confirmed that HIV does
not kill cells in the test tube.
of the HIV hypothesis cannot make HIV sound unusual enough, they
try instead to make other viruses sound like HIV. For example, a
retrovirus termed SIV is said to cause an "AIDS-like"
disease in monkeys. But with no long latent period, no wide variety
of diseases (no Kaposi's sarcoma or dementia), and where antibodies
protect against disease, we have great difficulty calling such conditions
When all else
fails, defenders of the virus-AIDS hypothesis resort to moving the
goalposts; rather than bringing the hypothesis into question, paradoxes
lead to painful contortions of its details. A latent period first
had to be invented, then extended to its present, and still growing,
total of 10 to 11 years. Antibodies had to be used, not merely to
indicate that the host carried the virus, but actually to predict
future disease. When Kaposi's sarcoma no longer even remotely correlated
with HIV, the Centers for Disease Control had to consider dropping
it from the AIDS list, rather than questioning whether AIDS was
even a single condition al all. In the past, virus-AIDS defenders
continually cited Africa as proof of their hypothesis; when we ourselves
began citing the actual data on Africa, opponents such as Fumento
turned around and adopted our previous position, that Africa proves
And when HIV
cannot meet Koch's postulates with AIDS, Whelan, Winkelstein, Temin,
and other virus-AIDS supporters casually try to abandon those time-tested,
commonsensical postulates. Contrary to often-stated claims, the
polio virus and the tuberculosis bacterium have indeed satisfied
Koch's criteria for their respective diseases. In polio, for example,
the virus can be isolated from the affected tissue in every case
of polio (postulate #1); the virus has been cultured (#2); the virus
causes disease in animals (apparently Winkelstein is unaware that
such experiments as Albert Sabin have caused poliomyelitis in monkeys
with injected polio virus); vaccines block the virus from causing
disease in humans (33); and the virus can always be reisolated (#4).
Until they are able to propose a clearly superior set of standards
for determining whether a virus causes a disease, HIV- AIDS proponents
are arbitrarily throwing out proven standards to accommodate HIV
raised by Orient about whether health-risk factors brought on AIDS-type
diseases in past decades. Searchers of the medical literature such
as Robert Root-Bernstein and ourselves, do reveal the association
of these conditions with such risks as drug use, surgical operations,
chemotherapy, and so forth. "Pneumocystis carinii" pneumonia,
for example, has generally been found in precisely such risk groups;
former California state legislator Paul Gann would never have been
considered unusual for developing such a condition after a traumatic
operation at an advanced age, but this was renamed AIDS because
he was also infected with HIV. And drug use has exploded in both
numbers and among of use, so that only within the last 10 or 15
years have noticeable numbers of diseased addicts begun showing
up in "inner-city hospitals."
Many who are
willing to question the HIV hypothesis are still not willing to
abandon the idea that AIDS is at least an infectious disease. McKenna,
Lo, Wear, and Konotey-Ahulu suggest that other infectious agents
may serve as co-factors, or even as primary agents of AIDS. However,
AIDS simply does not behave as any known infectious condition; it
is rigidly segregated in certain very specific risk groups, which
for the most part are themselves associated with drug use, and after
almost a decade over 90 percent of AIDS cases in the United States
continue to be found in males (over 80 percent of heavy drug users
are male). No precedent exists among infectious diseases for this
strange distribution. All known venereal diseases spread widely
through the population, including syphilis, herpes, gonorrhea, chlamydia,
etc. Mycoplasmas are also quite universal, and certainly do not
confine themselves so carefully to males or special risk groups
, so consistently, for a decade or more. Konotey-Ahulu's evidence
for AIDS as an infectious conation, mostly regarding urban prostitutes
in Africa, seems to us more probably related to drug use and other
western types of risk factors that have recently increased in availability
in those cities.
HOW TO RESOLVE
simple set of tests would quickly determine, once and for all, whether
HIV (or any virus) causes AIDS:
1) The virus
should be chemically active in more cells than the host can generate.
2) The symptoms
of the disease should occur within weeks or months after infection.
3) The disease
should spread relatively randomly among its potential hosts, rather
than being confined to highly specific groups.
produced by the immune system should be able to fight or completely
neutralize the disease.
5) A controlled
study, in which a group of people with the virus should be compared
to a group without, to see whether those with the virus develop
the sickness. The groups should be matched for all possible health
risk factors: equivalent types and amounts of drug use, use of antibiotics,
use of AZT, exposure to previous diseases, hemophilia, etc.
HIV, of course,
already fails points (1) through (4), and we have little trouble
anticipating the result of a controlled study.
But both of
us would be quite willing to carry out the Fumento test: if he will
arrange for sufficient national publicity, if he would be convinced
by our action, and if he will thereafter help us bring exposure
to our viewpoint, we will indeed be quite happy to have ourselves
publicly injected with HIV. Perhaps Fumento will also be willing
to check on our health status in the year 2000, or after whatever
additional time is eventually added to the virus's latent period.