The HIV-AIDS Myth
The Yin
& Yang of HIV
by Valendar F. Turner and Andrew McIntyre
Supporters
of the 'HIV causes AIDS' hypothesis cannot back up their claims with scientific
evidence, yet they continue to reject alternative explanations and promote
life-threatening drug treatments.
A theory is a good theory if it satisfies two requirements: It must
accurately describe a large class of observations on the basis of a model that
contains only a few arbitrary elements, and it must make definite predictions
about the results of future observations.
- Dr Stephen Hawking
The
notion that HIV/AIDS is infectious and sexually transmitted is based on a
relationship between antibodies claimed specifically induced by a retrovirus,
HIV, and particular diseases in certain risk groups. However, the HIV theory
has been challenged for well over a decade in many scientific publications,
principally by Peter Duesberg from the USA and Eleni Papadopulos-Eleopulos and
her colleagues in Perth, Western Australia.
Failure of
HIV/AIDS to spread beyond the original risk groups and particularly to Western
heterosexuals, especially non-drug-using prostitutes, signals that the HIV
theory of AIDS is in need of urgent reappraisal. This has serious implications
for both the way science has been conducted and for public health policy and
planning. The HIV theory has cost billions of dollars and locked in enormous
amount of energy in research by thousands of scientists worldwide. So far, it
has yet to save a single life.
There is an
urgent need to establish a truly independent and distinguished international
committee to review the current theories and those that challenge them. There
needs to be a co-operative but urgent reassessment of AIDS.
A Nobel Laureate Stirs
the Waters
In 1988, Dr
Kary Mullis, the 1993 Nobel Prize winner for Chemistry, was employed by
the US National Institutes for Health (NIH) to set up analyses for HIV testing.
When preparing his report, he asked a virologist colleague for a reference that
HIV is "the probable cause of AIDS". He was told he did not need one.
Mullis was surprised.1
"I
disagreed. It was totally remarkable to me that the individual who had
discovered the cause of a deadly and as-yet-uncured disease would not be
continually referenced in the scientific papers until that disease was cured
and forgotten... There had to be a published paper, or perhaps several of them,
which taken together indicated that HIV was the probable cause of AIDS."
Otherwise, as Mullis was forced to conclude: "The entire campaign against
a disease increasingly regarded as the twentieth-century Black Death was based
on a hypothesis whose origins no one could recall. That defied both scientific
and common sense."
A decade
later, Mullis was to write: "I finally understood why I was having so much
trouble finding the references that linked HIV to AIDS. There weren't
any."2
Indeed, an
interested non-specialist observer, armed with a few contacts and a good
library, merely has to scratch the surface to realise that the HIV theory of
AIDS begs many more questions than it answers.1-63*
The BEGINNINGS of AIDS
The few years
leading up to the AIDS era and the discovery of HIV are illuminating. It was a
time when a promiscuous minority of young, "liberated" gay men in a
few large American cities were increasingly developing previously uncommon
diseases such as fatal forms of the malignancy Kaposi's sarcoma and a fungal
pneumonia known as PCP.
At the time,
whilst it was reasonable to implicate an infectious microbe transmitted by
rampant, indiscriminant sexual practices interspersed with needle sharing and
drug taking, the fact that immune suppression had multiple causes was also
known in 1981. Some considered the diseases resulted from multiple assaults to
bodily functions caused by the many and varied diseases, toxins and treatments
that accompanied the gay and drug-taking lifestyle that had evolved during the
late 1970s.
Just how
extensive these multiple assaults were was indicated by the English journalist
Neville Hodgkinson, documenting the range of infections of just one homosexual,
the late Michael Callen, in his book, AIDS - The failure of contemporary
science: How a virus that never was deceived the world.29 Hodgkinson writes:
"From 1973, when he came out as a homosexual, to 1975, he only got
mononucleosis and non-specific urethritis (NSU). In 1975, he had his first bout
of gonorrhoea... But from there, it all began to snowball. 'First came hepatitis
A in 1976 [said Callen]. Then more NSU and gonorrhoea. In 1977, amoebas
[intestinal parasites] and hepatitis B...NSU and gonorrhoea. 1978: more
amoebas...my first case of shigella [and] more VD. Then in 1979, hepatitis a
third time...non-A, non-B...amoebas...giardias...a fissure [and] my first case
of syphilis. And of course, more gonorrhoea [penile, anal and oral]. In 1980:
the usual gonorrhoea, shigella twice, and more amoebas...'
Added to that
list were herpes simplex types I and II; venereal warts; salmonella; chlamydia;
cytomegalovirus (CMV); Epstein-Barr virus (EBV); mononucleosis; and finally
cryptosporidiosis ('a disease of cattle!')." Indeed, an early US Centers
for Disease Control (CDC) study confirmed that the first 100 men with AIDS had
a median lifetime number of 1,120 sexual partners.30 As Callen himself put it:
"By 1981, I got some combination of venereal diseases each and every time
I had sex."
Not
surprisingly, given the widespread belief of a causal relationship between
immunity and the maintenance of health, in 1981 the "new" disease
became known as Gay Related Immune Deficiency (GRID). In fact, none of the
diseases was new. Some were known to occur in drug addicts and haemophiliacs
long before the AIDS era.64, 65 What was "new" was their
exponentially escalating prevalence in gay men.
TECHNOLOGY & VIROLOGY
Coincidental
with the beginning of the AIDS era, a technique was developed to classify and count
the different types of lymphocyte white blood cells. It was noticed that some
AIDS patients had diminished numbers of the so-called T4 "helper"
cell subtype and, despite lack of proof, the cells were assumed to be dying at
the behest of an agent selectively targeting them. This became the
"hallmark" of AIDS as well, forming a measure of the amount of immune
deficiency. In turn, this "immune deficiency" (the "AID" in
AIDS) caused the diseases (the "S" in AIDS) that constitute the
clinical syndrome. The perceptions that T4 cells were dying and AIDS was infectious
led to the theory that AIDS is caused by a microbial organism.
Five years
prior to the AIDS era, a few laboratories around the world were drawing towards
the end of a fruitless search to prove a viral cause for human cancers. During
the 1970s, Dr Robert Gallo, the central figure as "co-discoverer" of
the AIDS virus, and his colleagues claimed to have discovered three human
retroviruses. (The name "retroviruses" arises because of the copying
of the RNA which forms the viral "genes" [the genome]
"backwards" into DNA - a direction contrary to that long considered
universal, that is, from DNA into RNA.)
In 1975, the
first human retrovirus, HL23V, was proposed to cause human leukaemia, but by
1980 was considered an embarrassing mistake - in fact, not to have ever
existed. Of the remaining two, one was postulated to cause a specific, though
rare, form of adult leukaemia, and the second remains orphaned without a
disease. What is significant is that the latter two retroviruses are said to
exhibit a liking for T4 lymphocytes.
This led
Donald Francis, Gallo and others to propose that an existing or closely related
retrovirus was the agent responsible for killing the T4 cells in AIDS patients.
When researchers actively sought and then discovered the same diseases in
individuals who were not gay, retroviruses, as well as retrovirologists,
received renewed interest and GRID became AIDS.
FIRST PROCLAMATIONS
In May 1983,
Professor Luc Montagnier and his colleagues at the Pasteur Institute in Paris
published a paper in Science, entitled "Isolation of a T-Lymphotrophic
Retrovirus from a Patient at Risk for Acquired Immune Deficiency Syndrome
(AIDS)".66 It is important to note that the first word in this paper,
"Isolation", serves as a signal that the researchers are claiming
proof for the existence of a new virus.
In the
interests of science, on several occasions Montagnier sent samples of his
tissue cultures to the Gallo laboratory in America, with the express
understanding that these "could be used for biomedical, biological and molecular
biological studies".67 However, Montagnier did not claim to have proven
his virus was the cause of AIDS, and the French discovery lay on the table
until May 1984 when Gallo and Popovic and their colleagues published four
papers, also in Science.68-71
On 23 April
1984, at a Washington press conference held two weeks before the papers were
published, Margaret Heckler, Secretary for Health and Human Services (HSS),
announced that Gallo and his co-workers had discovered the "probable"
cause of AIDS and had developed a sensitive blood test to detect the virus in
the body. A curative vaccine was predicted within two years. Inexplicably,
causation was proclaimed merely by association and despite
"isolation" of HIV in only 26 (i.e., 36 per cent) of Gallo's 72 AIDS
patients - barely a third. (The frequency of "isolation" is no better
today.72)
In 1985, the
Pasteur Institute alleged that Gallo had misappropriated their virus. The
ensuing conflict, which eventually reached the US courts, was settled by a
negotiated agreement signed in 1987 by Gallo and Montagnier as
"co-discoverers", and US President Reagan and French Premier Chirac.
Nevertheless, the matter drew the attention of John Crewdson, an investigative
journalist, and US Senator John Dingell. In November 1989, Crewdson published a
lengthy article in the Chicago Tribune newspaper, which provoked an internal
NIH enquiry into suspect data from Gallo's laboratory.
A draft report
of the formal investigation, written by the NIH Office of Scientific Integrity
(OSI), was published in September 1991, in which the principal author, Mikulas
Popovic, was accused "of misconduct for misstatements and
inaccuracies" that appeared in the first Science paper, and suggesting
that Gallo, as laboratory chief, "created and fostered conditions that
give rise to falsified/fabricated data and falsified reports".
The OSI's
final draft report, completed in January 1992, was immediately criticised, and
was followed by a review of the OSI report by the Office of Research Integrity
(ORI) which found Gallo guilty of scientific misconduct.
Nonetheless,
even after this long investigation and its conclusion, the US Government
withdrew its findings following Gallo's announcement of an appeal. Despite
this, in 1994, US officials credited Montagnier and his colleagues as the
discoverers of HIV and yielded the French a greater share of royalties from the
HIV antibody tests. In taking these unprecedented steps, Dr Harold Varmus, the
Director of the NIH, acknowledged that "scientists at the NIH used a virus
provided to them by Institut Pasteur to invent the American test kit".
This action scarcely vindicated the Dingell report which had concluded that the
settlement "barely managed to paper-over the glaring, unresolved
issues". Rather, it was the culmination of a cover-up where
"political and international reputational imperatives" at HHS
"assumed pre-eminence over scientific integrity", while defending
Gallo's claim became "tantamount to defending the US Government itself".73
According to
Eleopulos and her colleagues, regardless of the material uncovered by the OSI,
Gallo's data, which still remains the best of its kind, does not prove the
existence of HIV and, even if it did, nowhere in the papers is there proof that
HIV causes AIDS.16, 21
Enter Peter Duesberg
In December
1987, three and a half years after the Washington press conference, Professor Peter
Duesberg, virologist and molecular biologist at the University of California,
Berkeley, published an invited paper entitled "Retroviruses as Pathogens:
Expectations and Reality".3 Duesberg was a much fêted scientist,
considered to be "the golden boy of virology" and "the greatest
living retrovirologist". He had developed many of the laboratory
techniques for studying retroviruses and their genetic make-up, had discovered
cancer-causing genes, and was recipient of a $350,000 "outstanding
investigator" award from the NIH.
But Duesberg
dropped a bombshell. He asserted that, apart from the relatively few
cancer-causing retroviruses, the majority are virtually harmless. Duesberg
argued that HIV is neutralised by antibodies shortly after infection and thus
antibodies signal its containment. He also pointed to data proving that well,
sick or dying-from-AIDS, HIV-positive individuals contain insufficient amounts
of HIV to do harm. Even if HIV were to kill all the T4 cells it had infected
every 1 to 2 days, the number of T4 cells needing replacement approximated the
amount of blood shed by a man cutting himself shaving.
For the
protagonists, the low "viral burden" - that is, the amount of
"HIV DNA" in cells - was a fact that no one, not even Gallo, could
satisfactorily reconcile with an immunity-destroying pathogen killing gay men
within a year or two of diagnosis. However, rather than addressing this as a
scientific problem warranting dialogue with someone known to have considerable
knowledge of the subject, Duesberg's questions antagonised Gallo to the point
where he refused to discuss the matter. Meetings convened to deal with the
uncomfortable implications of Duesberg's paper were suddenly cancelled at the
highest level.
In 1989,
Duesberg presented further argument.4 HIV does not fulfil the postulates that
19th century bacteriologist Robert Koch had developed to prove a microbe causes
a disease. These four postulates are: (a) the organism must be present in all
cases of the disease; (b) it must be grown and then isolated in pure culture
from the cells of individuals with the disease; (c) it must reproduce the
disease when introduced into a susceptible host or experimental animals, (d)
from where it must once again be recovered.
According to
Duesberg: "From every angle, HIV
fails Koch's first postulate." The second postulate was fulfilled but
only by subjecting cells to drastic chemical manipulation that did not approach
conditions in vivo. (Eleopulos has argued how basic retrovirology has long
shown that oxidation which prevails in HIV/AIDS patients and their cell
cultures creates internal [endogenous] retroviruses in cells whose DNA was not
previously infected from the outside.12, 14, 15, 74, 75 One per- cent of human
DNA, that is, an amount 3,000 times larger than "HIV" DNA, is made up
of endogenous retroviral DNA.76)
The third
postulate failed because, as Duesberg points out: "During the past decade,
more than four hundred thousand AIDS patients have been treated and
investigated by a system of five million medical workers and AIDS researchers,
none of whom [has] been vaccinated against HIV... But ten years later there is
not even one case in the scientific literature of a health worker who ever
contracted presumably infectious AIDS from a patient... AIDS is not
infectious." Similarly, "nine years after the NIH first started
infecting chimpanzees with HIV - over 150 so far at a cost of $40,000-50,000
apiece", all "are still healthy".5**
In 1992,
Duesberg shifted focus from HIV to argue that "AIDS [is] acquired by drug
consumption and other noncontagious risk factors".5 Apart from illicit and
recreational drugs, Duesberg's list included the first "anti-retroviral"
drug, zidovudine (AZT). In other words, a specific treatment for HIV infection
was postulated to be a cause of AIDS.
Duesberg
continued to regard HIV as bona fide, but as an inert, harmless
"passenger" virus linked to AIDS only through the kinds of activity
associated with drug taking (including taking of prescribed drugs). Duesberg,
like others before him, pointed to the epidemiological data revealing a 50-fold
difference in the AIDS "attack rate" between various groups of
HIV-positive individuals, as well as the proclivity of certain AIDS diseases
for particular risk groups. Thus, 50 per cent of HIV-positive blood transfusion
recipients develop AIDS within one year (but so do 50 per cent of HIV
negatives) compared to 1 per cent of haemophiliacs. Kaposi's sarcoma was, for
all intents and purposes, confined to gay men.5,13,77 Thus, even if HIV were
necessary to cause AIDS, it could not be the only factor. However, accretion of
"co-factors" to the HIV theory rendered the significance of any particular
factor problematic. It was possible to argue that HIV may be only a minor
factor or, at least in the minds of Eleopulos and Duesberg, not a factor.
Apparently,
the role of HIV was also a problem for Montagnier. Although he wrote in Nature
in December 1984 that "all available data are consistent with the virus
being the causative agent of AIDS",78 in 1985 he expressed an opinion
impossible to reconcile with the HIV theory. "This syndrome occurs in a
minority of infected persons, who generally have in common a past of antigenic
stimulation and of immune depression before LAV [HIV] infection",79 that
is, cause after effect (italics ours). One must surmise that, within a year,
the discoverer of HIV was already hedging his bets. His recent interview with
the investigative journalist Djamel Tahi61 (see below) fuels such speculation.
ELEOPULOS and the PERTH
GROUP
Eleni
Papadopulos-Eleopulos' AIDS research began in 1981. In May 1986, she
submitted for publication a paper which refuted every step in the HIV theory,
including HIV itself. She also proposed an alternative, non-viral theory (of
which "Duesberg's" "Drugs/ AIDS hypothesis" is a subset),
and predicated non-toxic and relatively inexpensive treatments.
Her theory was
based on a general theory of cellular functioning, which she had formulated in
the 1970s as a basis for unravelling the genesis and improving the treatment of
cancer and to offer fresh insights into the pathogenesis of cardiovascular
diseases and ageing. Eleopulos postulates that normal cellular functioning is
determined by the level and oscillations of cellular redox23 (oxidation and its
chemical opposite, reduction). In her view, when oxidation is prolonged or
excessive, cells become abnormal, injured and susceptible to diseases.
Eleopulos had
noticed a link between the risk groups. Gay men, drug users and haemophiliacs
are exposed to chemical stressors in the form of semen, nitrites, illicit drugs
and factor VIII (the blood-clotting protein missing from and administered to
haemophiliacs). There is abundant evidence that these substances are potent
cellular oxidants.12 In Eleopulos' view, oxidative stress produces low numbers
of T4 cells and AIDS, as well as the phenomena inferred as proof for the
existence of HIV.
The ready
acceptance of the Montagnier/Gallo 1983/84 Science papers posed enormous
difficulties for Eleopulos in having her work published. Thus,
"Reappraisal of AIDS: Is the oxidation caused by the risk factors the
primary cause?" was twice rejected by Nature, eventually finding light of
day in Medical Hypotheses, twelve months after Duesberg.12 However, the editor
of this journal had also rejected the paper, only recanting after Eleopulos
worked for several months to convince him that equatorial Africa was not in the
grip of an epidemic of sexually transmitted immunodeficiency and thus not in
breach of her theory.11, 24, 63, 80
To paraphrase
the theoretical physicist Stephen Hawking: wrong predictions affirm bad
theories; correct predictions make them powerful. The HIV theory requires that
HIV causes all the AIDS-defining diseases and predicts that HIV/AIDS will
become a global epidemic via the oldest and most unstoppable of all human
activities. However, Kaposi's sarcoma, one of the two diseases for which the
HIV theory was proposed, is no longer attributed either directly or indirectly
(via AID) to HIV.12, 13, 54, 77, 81***
In the OECD
countries, the prediction of a sexual pandemic has failed completely. For
example, as of the beginning of 1998, 93 per cent of the cumulative deaths from
AIDS in Australia occurred in the original risk groups, that is, gay/bisexual
men, drug addicts and haemophiliacs. This observation fits the classic
demographic profile of non-infectious diseases such as pellagra, beri-beri and
scurvy which characteristically remain confined to their risk groups. All are
caused by vitamin deficiencies, but in the past were regarded as infectious and
sufferers were shunned and quarantined.
The HIV
protagonists also predicted a curative vaccine by the end of 1986 and an animal
model to prove the HIV theory beyond all doubt. Neither prediction has been
fulfilled. A vaccine is not envisaged until well into the next century,
possibly around 2010, and animals given "HIV" do not develop AIDS.
On the other
hand, the Eleopulos oxidative stress theory predicts the current demographic
data, an apparent loss of T4 cells, the risk from passive anal intercourse in
both sexes, HIV positive and AIDS patients being oxidised relative to normal
individuals, the amelioration of HIV/AIDS by the use of antioxidants, and a
non-infectious animal model. Every one of these predictions has materialised.
Oxidative stress is well established by hundreds of papers,14, 62, 82-84 so
much so that in the early 1990s the Pasteur Institute was advertising
international scholarships for study into the phenomenon. In fact, last year
Luc Montagnier became the principal editor of a 558-page book devoted to
oxidative stress in cancer, ageing and AIDS.85
The Eleopulos
theory predicts that a decline in T4 cells can occur without cellular death. In
fact, according to the Perth group, there is no evidence to support the notion
that T4 cells are dead or that "HIV" kills such cells. In T4 cell
cultures, the same number of T4 cells "disappear", regardless of
whether one adds "HIV" or merely the chemical stimulants obligatory
to "grow" the "HIV".86 Neither is there proof that low
numbers of T4 cells are either necessary or sufficient to produce the clinical
syndrome.9,12,14 This is a view recently expressed by leading HIV/AIDS
scientists such as Dr Arthur Anderson from the US Army Medical Research
Institute of Infectious Disease87 and Dr Zvi Grossman at the University of Tel
Aviv.88
In other
words, the central tenet of the HIV theory - virus-induced killing of immune
cells leading to AIDS - is now being questioned by HIV/AIDS experts themselves.
Nonetheless, and despite so much evidence to the contrary, the orthodox view
remains entrenched. In fact, since 1993, the low number of T4 cells has been enshrined
in the 1993 CDC AIDS definition whereby AIDS can be diagnosed without a
disease. Just as "co-factors" were proposed to rescue the HIV theory
in the mid 1980s, in July 1998 Chen and colleagues from the UCLA AIDS
Institute, School of Medicine, Los Angeles, reported evidence that
"naturally non-infectious virus" or virus "rendered
defective" by "anti-HIV" drugs could still contribute to the
loss of T4 cells throughout the course of HIV disease.89 In other words,
"alive" or "dead", HIV causes immune deficiency. Such a
proposal does not augur well for the use or continued development of
"anti-HIV" drugs.
Consistent
also with the Eleopulos oxidative stress theory is the direct relationship
between high frequencies of passive anal intercourse and the development of
AIDS, as well as the fact that the only animal model of AIDS is non-infectious.
Mice repeatedly injected with foreign cellular proteins develop a dramatic
depletion of T4 cells and Kaposi's sarcoma-like tumours, and
"abundant" retrovirus-like particles appear in their spleens.90 Thus
AIDS diseases are followed by the production of retrovirus-like particles, and
not the other way around.
To the
uninitiated this may seem perplexing, but it is well recognised that retroviral
particles appear de novo in cell cultures not previously infected, because all
cells contain retroviral information carried in the germ line DNA.76 Indeed,
according to distinguished retrovirologists such as Weiss and Temin, new
retroviral DNA arises by rearrangement of cellular DNA, caused by many factors
including pathological processes - a view that concedes retroviruses an effect
and not the cause of diseases.74, 75
The RISE and FALL of
"ANTI-HIV" DRUGS
It would take
a second article to discuss AZT and the many other "anti-HIV" drugs. Suffice it
to say there is no scientific proof that such drugs kill "HIV" or
cure AIDS, but there is ample evidence they are harmful.1, 53, 56, 91
In 1994, a
double-blind randomised comparison of two policies of AZT treatment (immediate
and deferred) was reported (the Concorde trial). This involved 1,749
symptom-free, HIV-infected individuals from centres in the UK, Ireland and
France. The 347 clinical endpoints (AIDS and death) outnumbered the total of
those in all other published trials in symptom-free and early symptomatic
infection. The results showed "there was no statistically significant
difference in clinical outcome between the two therapeutic policies".92 In
1995, extended results of Concorde showed a significant increased risk of death
among the patients treated early.
However,
despite these data, despite disclaimers that patients treated with AZT may
continue to develop the AIDS diseases, that the side effects of AZT may mimic
AIDS, and that AZT given to non-HIV-infected babies causes the AIDS-defining
pneumonia, PCP,93 AZT continues to be the most commonly prescribed anti-HIV
drug.
Dr Donald
Abrams, Professor of Medicine and Director of the AIDS program at San Francisco
General Hospital, said: "I have a large population of people who have
chosen not to take any anti-retrovirals... I've been following them since the
very beginning... They've watched all of their friends go on the antiviral
bandwagon and die."94
Indeed, even
an elementary study of the pharmacological literature reveals that AZT cannot
be an anti-HIV drug; it is toxic to all cells.91 In fact, what unites long-term
survivors of AIDS is their resolve not to take
"anti-retrovirals".95-97
In mid-1996,
the latest drugs, the "protease inhibitors" (PIs), were introduced.
These are prescribed as one of up to 250 possible combinations of
"cocktails" with AZT or similar drugs as "highly active
anti-retroviral therapy" (HAART). Detailed data on these drugs, of the
kind usually reserved for medical practitioners, appear regularly in glossy,
multi-page advertisements in gay men's magazines.
At the July
1996 11th International AIDS Conference, Time magazine Man of the Year David Ho
predicted that scientists would "find new drugs to wipe HIV out of the
body within three years, possibly within just one".98 At the July 1998
XIIth AIDS conference, Ho stated it will take at least 10 years of intense
combination drug therapy to kill off all the HIV in an infected person's body,
but that a sizeable percentage of HIV patients will never get close. Many
patients cannot tolerate the untoward effects of these "cocktails",
and measurements show that the DNA "viral" burden does not decrease
significantly.99-102 According to Kaufmann et al.: "49% of people taking
HAART, who were followed by the Swiss HIV Cohort Study, did not have viral
suppression, and similar data are emerging from other centres."103
In the May
1998 Proceedings of the National Academy of Sciences, Dr William Paul, former
Director of the National Institutes of Health's Office of AIDS Research, wrote:
"...no matter how long a person is treated with anti-HIV drugs, there will
always be new viruses...you will have to be treated forever... No one is
getting cured... This bodes extremely poorly for combination therapy as
something curative..."88
Dr Michael
Saag, at the University of Alabama, Birmingham, USA, is responsible for the
treatment of over 1,000 AIDS patients. His treatment is state-of-the-art and
his clinic is sought- after by pharmaceutical companies to conduct trials on
their newest compounds. In a recent interview, Dr Saag said: "Perhaps the
biggest difference between the cure paradigm and whatever paradigm we're in now
is, we now should expect failure with whatever [HAART cocktails] we first use.
We should plan on it. We should prepare for it. Clinicians should expect
failure." Saag warns the HAART "'dam' is already leaking and there's
high danger of it collapsing altogether. Failures are occuring right and
left." Speaking about his dying patients: "They aren't dying of
traditionally defined AIDS illness... I don't know what they're dying of, but
they are dying. They're just wasting and dying... It is sobering...while we are
making good guesses, they are just guesses. We don't know what we are
doing."104
Given the
toxicity of these drugs, it is unlikely anyone can tolerate taking them for
more than a few years. If this outlook is gloomy for HIV/AIDS sufferers, it is
even worse considering there is no substantial, alternative therapeutic
strategy anywhere on the horizon.
The futility
of all "anti-HIV" drugs, past, present and future, is best
highlighted in a June 1998 interview by Dr Harold Varmus, Nobel Laureate
retrovirologist and Director of the National Institutes of Health: "Trying
to rid the body of a virus whose genome is incorporated into the host genome
may be impossible."105
The DEMISE of SCIENTIFIC
DEMOCRACY
The longevity
of the HIV theory has been considerably boosted by the virtual refusal of editors
of leading medical journals to publish any material which takes HIV to task.
Without these data, and the stamp of approval engendered by such publication,
it is almost impossible for the debate to reach the ears of those who matter
the most: clinicians and their patients. Like generals directing wars, the
remoteness of editors begets an objectivity which, while essential to clear
thinking, militates against an appreciation of the profound responsibilities
editors hold at the bedside.
Ultimately,
although the HIV theory is manifoldly problematic, physicians, patients,
relatives, politicians, journalists and the tax-paying public are
systematically denied knowledge of its existence and substance. Not only is
there is a total absence anywhere of a disinterested, adjudicated debate, but
individuals, whose only motivation is to contribute to solving a disease
claimed to afflict millions of people, find themselves censored. For example,
Sir John Maddox, former editor of the world's most prestigious science journal,
Nature, denied Duesberg the right of reply on issues he raised because his
views give "many infected people the belief that HIV infection is not in
itself the calamity it is likely to prove".29 Yet, in a recent edition of
the same journal, but in another context, there is a claim that "the voice
of sceptics may grow tiresome, but the mainstream is in trouble if it cannot
win a public debate with them".
Officials at
the Berlin 10th International AIDS Conference confiscated Dutch AIDS analyst
Robert Laarhoven's press pass and threatened him with expulsion from Germany
for "criminal trespass" because he placed copies of the dissident
journal Rethinking AIDS on an "unauthorised" table.
Nature has
repeatedly rejected every paper and letter submitted by Eleopulos and her
colleagues since 1986, without providing a single scientific reason and
invariably citing space constraints in the journal. Not even the profound
implications of the Tahi/Montagnier interview are of any apparent concern to
Nature. Professor John Kaldor, one of Australia's foremost "established
experts" on AIDS, admits that dissidents "intersperse their cases
with grains of fact".106 However, because of Kaldor and colleagues'
"strong instinct not to dignify the sceptics' arguments by attempting to
refute them", arguments based on these "grains of fact" and many
other data remain unanswered and unresolved.
When
put to the test, conventional HIV/AIDS theory is at odds with the clinical
evidence. Is "purified HIV" no more than a tangle of cellular debris?
The real purpose of
scientific method is to make sure Nature hasn't misled you into thinking
something you don't actually know... One logical slip and an entire scientific
edifice comes tumbling down. One false deduction about the machine and you can
get hung up indefinitely.
- Robert Pirsig, Zen and the Art of Motorcycle
Maintenance
SOME SCIENTIFIC PROBLEMS with the HIV THEORY
The theory vs the definition
The central premise of the HIV theory of AIDS is that there exists a unique
retrovirus, transmissible via blood and sexual secretions, which induces specific
antibodies and kills T4 cells whose relative absence then causes the appearance
of approximately 30 diseases which constitute the clinical syndrome. The
theory, however, is rendered completely contradictory by the official AIDS
definition used clinically.
In Australia,
an individual is diagnosed as having AIDS if he or she fulfills the criteria
set out in the latest (1993) revision of the US "CDC surveillance case
definition for AIDS".107 (Other definitions in use around the world make
scientific comparisons almost impossible. In Africa, AIDS is diagnosed on
symptoms and without blood tests.108) Since from 1985 the Centers for Disease
Control "accepts" HIV as the cause of AIDS, it should not be possible
to diagnose AIDS by any means inconsistent with the HIV theory. However, even a
cursory reading of the 1993 definition reveals AIDS can be diagnosed - with the
imprimatur of the CDC - with Kaposi's sarcoma (which even Gallo54 accepts is
not caused by HIV), in the absence of immune deficiency, "without laboratory
evidence of HIV infection" and, extraordinarily, "in the presence
of negative results for HIV infection"109 (italics ours).
Sexual transmission
HIV/AIDS is claimed to be bidirectionally sexually transmitted. Data to support
this claim are based not upon microbial isolation and contact tracing, as is
the orthodox practice for proving diseases are infectious and sexually
transmitted, but on mostly retrospective studies of highly selected groups of
individuals - including homosexual and bisexual men, heterosexual men and women
including prostitutes - for antibodies in blood which react with certain
proteins deemed "HIV-specific". Included in these studies are
estimations of risk factors for the specific sexual practices of
penile-insertive, vaginal, anal-receptive and oral-receptive intercourse.
Homosexual
men
In 1984, Gallo and his colleagues showed that "Of eight different sexual
acts, a positive HIV antibody test correlated only with receptive anal
intercourse".110 They also found that the more often a homosexual man had
insertive anal intercourse, the less likely he was to become HIV-positive. This
is incompatible with an infectious cause. In 1986, Gallo and his colleagues
reported they "found no evidence that other forms of sexual activity
contribute to the risk" of HIV seroconversion in homosexual men.111
In an
extensive review of 25 studies of homosexual men reported in 1994 by Caceres
and van Griensven, the authors concluded that "no or no consistent risk of
the acquisition of HIV-1 infection has been reported regarding insertive
intercourse".112
In the West,
the largest and most judiciously conducted prospective epidemiological studies,
such as the Multicenter AIDS Cohort Study (MACS) of 4,954 gay men,113 have
proven beyond all reasonable doubt that in homosexual men the only significant
sexual act related to becoming HIV-antibody-positive is receptive anal
intercourse. Thus, in gay men, AIDS may be likened to the non-infectious
condition, pregnancy. It is acquired by the passive partner but is not
transmitted to the active partner.
Significantly,
the MACS also showed that once a homosexual man becomes HIV-positive,
progression to AIDS is further determined by the amount of passive anal
intercourse sustained after "infection". This is contrary to all that
is known about infectious diseases. Infection, not repeated infections, causes
disease. Indeed, the Royal Australasian College of Surgeons (RACS) considers
HIV-positive surgeons to be "infectious" and that they "should
not perform invasive procedures or operations", but "they may provide
these services to patients who have the same infection".114
Heterosexuals
The largest and best-conducted studies in heterosexuals, including the European
Study Group,115 showed that, for women, the only sexual practice leading to an
increased risk of becoming HIV-antibody-positive is anal intercourse. The
unidirectional transmission of "HIV" observed in OECD countries is
supported by Nancy Padian's 10-year study of heterosexual couples (1986-1996).
There were two parts to this study: one cross-sectional, the other prospective.
In the
cross-sectional study, "The constant per-contact infectivity for
male-to-female transmission was estimated to be 0.0009 [1 in 1,111]". The
risk factors for the women were: (i) anal intercourse; (ii) having partners who
acquired this infection through drug use (Padian says this means the women may
also be IV drug users); (iii) the presence of STDs (antibodies to their
causative agents may react in an "HIV" antibody test).15, 20 Of the HIV-negative
male partners of 82 HIV-positive female cases, only two became HIV-positive -
but under circumstances that Padian considered ambiguous.
In the
prospective study, starting in 1990, 175 HIV-discordant couples were followed
for approximately 282 couple-years. At entry to the study, one third used
condoms consistently and, in the six months prior to their last follow-up
visit, 26 per cent of couples consistently failed to use condoms. There were no
seroconversions after entry, including the 47 couples not using condoms
consistently. Based on the 2 in 86 men who became HIV-positive in the early
study, the risk to a non-infected male from his HIV-positive female partner was
reported to be in the order of 1 in 9,000 per contact. From this statistic one
can calculate that, on average, a male would need to have 6,000 sexual contacts
with an infected female to achieve a 50 per cent chance of becoming
HIV-positive. If sexual intercourse were to commence at age 20 and average
three times weekly, this would occupy a lifetime.57, 116
Female
Prostitutes
The notion that HIV is a virus which "does not discriminate" is also
markedly inconsistent with the data obtained from studies of female
prostitutes. Even if by some unknown means a sexually transmitted infectious
agent found its way into the promiscuous portion of the gay male population in
certain large cities in the United States in the late 1970s (as is widely
accepted), and given the facts that prostitutes are frequented by bisexual men
and that, at the very earliest, "safe" sexual practices date from
1985, one would have expected HIV/AIDS to have spread rapidly through
prostitutes and thence to the general community. However, the prevalence of
"HIV" antibodies amongst prostitutes is almost entirely confined to
those who are drug users. Virtually all other prostitutes have not been, and
are not becoming, HIV-positive.
In September
1985, 56 non-intravenous drug using (IVDU) prostitutes were tested "...in
the rue Saint-Denis, the most notorious street in Paris for prostitution. More
than a thousand prostitutes work in this area... These women, aged 18-60, have
sexual intercourse 15-25 times daily and do not routinely use protection."
None was positive.118
In Copenhagen,
101 non-IVDU prostitutes, a quarter of whom "suspected that up to one
fifth of their clients were homosexual or bisexual", were tested during
August-October 1985. The median numbers of sexual encounters per week was
twenty. None was positive.118
In 1985, 132
prostitutes (and 55 non-prostitutes) who attended a Sydney STD clinic were
tested for HIV antibodies. The average number of sexual partners (clients and
lovers) in the previous month was 24.5. When an estimate was made to separate
clients and lovers, the median number of sexual contacts per year rose from 175
to 450. The partners of only 14 prostitutes (11%) used condoms at all, and 49%
of their partners used condoms in fewer than 20% of encounters. No women were
HIV-positive.119
The same
Australian clinic repeatedly tested an additional 491 prostitutes who attended
between 1986 and 1988. Of 231 out of the 491 prostitutes surveyed, 19%
"had bisexual non-paying partners and 21% had partners who injected drugs.
Sixty-nine per cent always used condoms for vaginal intercourse with paying
clients, but they were rarely used with non-paying partners. Condoms were
rarely used by those clients and/or partners for the 18% of prostitutes
practising anal intercourse." No women were HIV-positive.
At the time of
this report, a decade into the AIDS era, the authors commented that "there
has been no documented case of a female prostitute in Australia becoming
infected with HIV through sexual intercourse" (italics ours). Yet,
these investigators from the Sydney Sexual Health Centre concluded that
"there are still many women working as prostitutes in Sydney who remain
seriously at risk of HIV infection".120
In Spain, of
519 non-IVDU prostitutes tested between May 1989 and December 1990, only 12
(2.3%) had a positive test, which was "only slightly higher than that
reported five years ago in similar surveys". Some prostitutes had as many
as 600 partners a month, and the development of a positive antibody test was
directly related to the practice of anal intercourse. The authors also noted
that "a more striking and disappointing finding was the low proportion of
prostitutes who used condoms at all times, despite the several mass-media AIDS
prevention campaigns that have been carried out in Spain".121
Similar data
from two Scottish studies,122 the 1993 European Working Group on HIV Infection
in Female Prostitutes study,123 and a 1994 report on 53,903 prostitutes working
in the Philippines and tested between 1985 to 1992, confirm that non-IVDU
prostitutes remain virtually devoid of HIV infection. For example, in the latter
study, only 72 women (0.01%) were found to be HIV-positive.
In studies
where there appears to be a high incidence of HIV amongst prostitutes, there
are uncertainties that defy explanation. For example, although "HIV has
been present in the commercial sex work networks in the Philippines and
Indonesia for almost as long as it has been in Thailand and Cambodia", the
prevalence of HIV in the former is 0.13% and 0.02% respectively and 18.8% and
40% in the latter.124
If these are
accurate data, the discrepancy defies epidemiological explanation and has
indeed baffled the experts, although the latter postulate "behavioural
factors", such as one country's prostitutes and clients being considerably
more or less sexually active than another. However, one could also pose another
question. What are the "HIV" antibody tests actually measuring? Be
that as it may, since 5,674 (44%) and 4,360 (34%) of the 12,785 Cambodian
"HIV and AIDS Case Reports" till 31 December 1997 are listed as
"Unknown" in gender and age respectively,125 data collection, at
least by the World Health Organization in Cambodia, must be regarded as
problematic.
Contradictions
Why should HIV avoid non-drug-using prostitutes? If female prostitutes who do not
use drugs do not become HIV-infected despite being "seriously at risk of
HIV infection", what is the risk of infection to the majority of
Australian women who are neither drug users nor prostitutes? According to data
from the National Centre in HIV Epidemiology and Clinical Research, vanishingly
little. A 1989 study testing 10,217 blood samples of newborn babies
(unambiguous evidence of unprotected heterosexual intercourse) found no babies
and thus, presumably, no mothers HIV-positive.126 If such women remain non-
infected, how do their non-drug-using, male heterosexual partners become
infected with HIV?
According to
Simon Wain-Hobson, a leading HIV expert from the Pasteur Institute, "a
virus's job" is to spread. "If you don't spread, you're dead".
The "overwhelming" evidence from studies both in homosexual men and
heterosexuals is that HIV/AIDS is not bidirectionally sexually transmitted. In
the whole history of medicine there has never been such a phenomenon. Since
microbes rely on person-to-person spread for their survival, it is impossible to
claim from epidemiological data that HIV/AIDS is an infectious, sexually
transmitted disease. Indeed, Professor Stuart Brody, from the University of
Tübingen, has argued that physicians ignore the actual heterosexual data and
instead promote the politically correct idea that everyone is at risk.
"Ideological knowledge about AIDS is far more likely to filter through
society than scientific knowledge."37
The HIV WESTERN BLOT
TEST
The HIV Western blot test consists of a thin nitrocellulose strip in which are
embedded proteins claimed to be unique to HIV. Each protein is labelled with
a "p" followed by its molecular weight in thousands. Serum is added
to the strip and, if there are antibodies to a particular protein, this band
will "light up". The HIV Western blot is not standardised, and
thus, around the world, different combinations of bands are considered
positive. Hence a positive test in one country is not positive in another. An
African would not be positive in Australia. A person from the MACS would not
be positive anywhere in the world, including Africa. Yet the HIV Western blot
is considered to be highly specific and is considered synonymous with HIV
infection. |
 |
Key: AFR
= Africa;1 AUS = Australia;2 FDA = US Food and Drug Administration;3 RCX = US
Red Cross;3 CDC = US Centers for Disease Control;3 CON = US Consortium for
Retrovirus Serology Standardization;3
GER = Germany; UK = United Kingdom; FRA = France; MAC = US Multicenter AIDS
Cohort Study 1983-1992
According to
data presented in Lundberg et al.,3 when the US FDA criteria are used to
interpret the HIV Western blot, less than 50% of US AIDS patients are
HIV-positive, whereas 10% of persons not at risk of AIDS are also
HIV-positive by the same criteria.
Note:
In February 1993, the US FDA relaxed its stringent criteria in order to
"reduce the number of HIV-1 seroindeterminate Western blot
interpretations"; that is, to increase the number of HIV-positive individuals.4
Endnotes
1. WHO (1990), "Acquired Immunodeficiency Syndrome (AIDS). Proposed
criteria for interpreting results from Western blot assays for HIV-1, HIV-2
and HTLV-I/HTLV-II", Weekly Epidem. Rec 65:281-298.
2. Healy, D.S., Maskill, W.J., Howard, T.S. et al. (1992), "HIV-1
Western blot: development and assessment of testing to resolve indeterminate
reactivity", AIDS 6:629-633.
3. Lundberg, G.D. (1988), "Serological Diagnosis of Human
Immunodeficiency Virus Infection by Western Blot Testing", JAMA 260:674-679.
4. Kleinman, S., Busch, M.P., Hall, L. et al. (1998), "False-positive
HIV-1 test results in a low-risk screening setting of voluntary blood
donation", JAMA 280:1080-1083. |
THE DIAGNOSIS of
"HIV" INFECTION
The HIV antibody tests
There are two "HIV" antibody tests in common use: the ELISA and
Western blot (WB). The ELISA causes a colour change when a mixture of
"HIV" proteins reacts with antibodies in serum from a patient. In the
WB, the "HIV" proteins are first separated along the length of a
nitrocellulose strip. This enables individual reactions to the 10 or so
"HIV" proteins to be visualised as a series of darkened
"bands". The Western blot test is used to "confirm"
repeatedly positive ELISAs because experts agree that the ELISA
"overreacts"; that is, it is insufficiently specific.×
Prior to 1987,
one "HIV-specific" WB band was considered proof of HIV infection.
However, since 15%-25% of healthy, no-risk individuals have
"HIV-specific" WB bands,127, 128 it became necessary to redefine a
positive WB by adding extra and selecting particular bands, otherwise at least
one in every seven people would be diagnosed as infected with HIV.
(Notwithstanding, in the MACS, one band remained proof of HIV infection in
homosexual men until 1990.129) On the other hand, although AIDS in Europe and
the US began to decline in 1987,130, 131 this trend was countered by the
addition of more and more diseases and, most recently, mere laboratory
abnormalities132 to each revision (1985, 1987, 1993) of the first, 1982 CDC
definition.
The net effect
of these changes was to maintain a correlation between "HIV"
antibodies and "AIDS" amongst the "risk" groups, while the
risk of an HIV/AIDS diagnosis outside these groups remained slight. This was
further accentuated by avoiding testing outside the risk groups. However, when
such studies were performed amongst 89,547 anonymously tested blood specimens
from 26 US hospital patients meticulously chosen to be at no risk of AIDS,
0.7%-21.7% of men and 0.0%-7.8% of women aged 25 to 44 years were found to be
HIV-WB-positive.133 (It is estimated that approximately 1% of men are
homosexual. Also, at the five hospitals with the highest rates of HIV
antibodies, one third of positive tests were in women. Yet men vastly outnumber
women as AIDS patients.)
In addition,
the US Consortium for Retrovirus Serology Standardization reported that 127
(10%) of 1,306 individuals at "low risk" for AIDS, including
"specimens from blood donor centers", had a positive HIV antibody
test by the "most stringent" US WB criteria.127
Thus the
correlation of "HIV" antibodies with AIDS - which experts accept as
the only in vivo proof that HIV causes AIDS - is not a statistic related to the
natural, unbridled activity of a virus, but is instead a contrivance generated
by mankind. Not only does correlation never prove causation, the artificiality
of this particular "correlation" severely compromises its scientific
analysis.
One of the
most bizarre aspects of the HIV/AIDS theory is that different laboratories,
institutions and countries define different sets of WB bands as a positive test
(see chart on previous page). The global variation in interpretive criteria
means that in Australia, for example, a positive test requires particular sets
of four bands. In the USA, different sets of two or three suffice, which may or
may not include the bands required in Australia. In Africa, only one designated
set of two is required. Put simply, this means that the same person tested in
three cities on the same day may or may not be HIV-infected.
If the
diagnosis of HIV infection were a game of poker, a flush would require five
cards the same suit in one country, but only one or two elsewhere. A virus
cannot behave in this manner, but according to the HIV test, which is claimed
to have a specificity of 99.999%,134 it does. As incomprehensible as this
appears, further difficulties remain. For example, an Australian tested in
Australia with one or two "HIV- specific" bands would not be reported
as HIV-infected.109 Clearly, however, there must be a reason why an uninfected
individual, such as a healthy blood donor or military recruit, can possess any,
even one, "HIV-specific" band. According to the experts, these bands
are caused by cross-reacting, that is, "false", "non-HIV" antibodies
which react with the "HIV" proteins. Thus it is axiomatic that an
antibody which reacts with a particular protein is not necessarily an antibody
which the immune system has generated specifically in response to that protein.
The Australian
National HIV Reference Laboratory (NRL) concedes that "False reactivity
may be to one or more [HIV] protein bands and is common (20%-25% of
anti-HIV-negative blood donors [will] exhibit one or more bands on a
WB)".128 However, Eleopulos argues that if "non-HIV" antibodies
cause "one or more protein bands", then why are they not able to
cause four or five? Or all ten? On what basis do experts assert which
antibodies are "false" and which are "true"? Or, how do the
same three bands, caused by "false", non-"HIV" antibodies,
become "true" when accompanied by one extra? On what basis do experts
assert there are any "true" HIV antibodies? If the Australian
traveller were to be tested in the USA, where two or three bands are sufficient
to diagnose HIV infection, are his antibodies "false" in Australia
but "true" as his aeroplane touches down in Los Angeles?
In 1994, one
of us (VFT) wrote to the Medical Journal of Australia, seeking
justification of both the Australian criteria for a positive Western blot test
and the global variability.28 The response by Dr Elizabeth Dax of the NRL135
did not answer either question, and subsequent correspondence failed to pass
the editorial staff at the same journal. When the same questions were later put
via the offices of Senator Chris Ellison, the first question was again
unanswered, and the widely different criteria between Australia and Africa were
justified on the basis that, in Africa, "comparatively false reactivity is
far less common [than in Australia] so that interpretation criteria to define
[true] positivity may be less strict".128 However, no scientist can make
such a claim without data.
All antibody
tests are subject to the vagaries of cross-reactions, and the only way to
calculate the incidences of "true" and "false" antibodies
is to scrutinise reactions against what the test is purportedly meant to
measure, that is, against HIV itself.
HIV isolation
is the only "gold standard" by which the specificity of the
antibodies can be determined, and this must be evaluated before the test is
introduced into clinical practice.
However,
despite the WB test being in widespread use and "a stalwart"135 of
HIV testing, these data have never been reported by the NRL or any other
laboratory. Even without such evidence - since (a) the NRL concedes that
cross-reacting antibodies cause misleading reactions in the WB in one quarter
of healthy Australians, and (b) unlike Australians, Africans (similar to the
AIDS risk groups) are exposed to a multitude of infectious agents producing
myriad antibodies, each capable of cross-reactions - "false
reactivity" will be much higher in Africa where the WB criteria should be
the most stringent. If "HIV" antibodies indeed prove that one third
of heterosexual adults in certain central and eastern African countries are
infected with HIV, "life in these countries must be one endless
orgy".39
If the
proteins used in the HIV ELISA and WB tests are unique constituents of an
exogenous retrovirus, and if such a virus induces specific antibodies, we would
never expect to find such antibodies in the absence of HIV. Yet, in addition to
the circumstances above, there are numerous others where antibodies which react
with the "HIV-specific" proteins arise where HIV/AIDS experts concede
there is no HIV. These include healthy mice injected with lymphocytes of
similar mice136 or bacterial extracts (V. Colizzi et al., personal
communication); following the transfusions of HIV-free blood137 or a person's
own irradiated blood138; and 72 out of 144 dogs tested at a veterinary clinic
in Davis, California, USA.139 In addition, antibodies to the microbes which
cause the fungal and mycobacterial diseases affecting 90% of AIDS patients
react with the "HIV-specific" proteins.20, 140
This year it
was reported that 35% of patients with primary biliary cirrhosis, 39% of
patients with other biliary disorders, 29% of those with lupus, 60% of patients
with hepatitis B, 35% with hepatitis C - all non-HIV, non-AIDS diseases - have
antibodies to the "HIV" p24 "core" protein.141 Until 1990,
an unknown number of the 4,954 homosexual men in the MACS were diagnosed
HIV-infected on the basis of an antibody to the "HIV-specific" p24
protein, that is, with one WB band. Why do not all similar tests prove
infection with HIV? Why are gay men with a single p24 band infected with a
deadly virus, while biliary and liver disease patients with the same band are
not? Why were the criteria for diagnosing HIV infection set less rigorously for
homosexual men and Africans? And if HIV antibodies are specific and HIV
infection is "for life", why do reformed drug addicts, leading
healthy lives, lose their HIV anti-bodies?142
Although all
HIV experts accept cross-reactivity in HIV antibody testing, in 1993 the New
South Wales Department of Health interpreted the discovery of "HIV"
antibodies in four women as "compelling evidence" for transmission of
HIV from a homosexual man during the course of minor, office surgery in
1989.143 However, there was no proof that the man was HIV-infected at the time
of surgery, or that any of the four women were operated on after the man.
This report
remains the only one of its kind in the world, and it immediately led to the
establishment of a special committee of the Royal Australasian College of
Surgeons which wrote to all College Fellows, inviting submissions upon the
matter. But, rather than seizing upon the rarity of the event and following
advice urging a formal scientific enquiry into whether "HIV"
antibodies are caused by infection with a retrovirus,144 the College accepted
these data as proof of cross-infection but concluded, "The mode of
transmission is unknown".114 ××
Unlike
HIV/AIDS experts, who claim the specificity of the HIV antibody test is
99.999%, one manufacturer of HIV antibody tests states in the package insert:
"At present there is no recognized standard for establishing the presence
or absence of HIV-1 antibody in human blood. Therefore sensitivity was computed
on the clinical diagnosis of AIDS, and specificity based on random [healthy
blood] donors..."145 The latter were chosen as de facto non-HIV-infected
for the purposes of determining how many tests are false positives. However, by
this "reasoning", since the majority of HIV-positive individuals are
healthy, they cannot be infected. Thus the WHO146 predictions of a global
pandemic are patently untrue.
Discovery consists of
seeing what everybody has seen and thinking what nobody has thought.
- Albert Szent-Györgyi, Physician and Nobel Laureate
The DIAGNOSIS of
"HIV" INFECTION
What proof is there for the existence of HIV?
Scientific
evidence for the existence of a retrovirus must be consistent with the
definition of a retrovirus as a particular kind of replicating, microscopic
particle. Thus researchers must demonstrate the correct size, shape and
construction of particles; that these particles have been purified and analysed
and contain RNA as well as an enzyme (reverse transcriptase) that makes DNA
from RNA; and that the particles are infectious - that is, when pure particles
are introduced into fresh cell cultures, identical progeny appear. The latter
necessitates a second round of purification and analysis. Indeed, although this
method is entirely logical and was deemed essential at a meeting held at the
Pasteur Institute in 1973,147, 148 it has been ignored by all HIV researchers.
Although there
are electron microscope (EM) photographs from unpurified cell cultures of
particles purported to be HIV particles, it was not until March 1997 that EMs
of "purified HIV" were published.149, 150 Yet such data is the first,
most essential step in attempts to prove particles are a virus, and for
subsequent extraction of constituents for analysis and use as diagnostic
reagents. These long-awaited micrographs reveal "purified HIV" to be
a tangle of cellular debris. Scattered amongst this are scant particles which,
without evidence, the authors claim are the HIV particles and which
"copurify" (sic) with the cellular material. Close examination of
these particles as well as other evidence in the papers shows they are too
large, wrongly shaped, have too high a mass, and are devoid of knobs that HIV
experts unanimously assert are absolutely essential for the "HIV"
particle to cause infection. It is from this material that HIV/AIDS experts and
biotechnology companies obtain proteins and RNA to use in tests to pronounce
humans infected with a unique, exogenous, AIDS-causing microbe.
On 17 July
1997, the French investigative television journalist Djamel Tahi interviewed
Professor Luc Montagnier in camera at the Pasteur Institute in Paris.
Montagnier was asked: "Why do the EM photographs published by you [in
1983] come from the culture and not the purification?" His reply was:
"There was so little production of virus it was impossible to see what
might be in a concentrate of the virus from the gradient ["pure
virus"]. There was not enough virus to do that. Of course one looked for
it, one looked for it in the tissues at the start; likewise the biopsy. We saw
some particles but they did not have the morphology typical of
retroviruses" [italics ours].61 Questioned about the Gallo group,
Montagnier replied: "Gallo? I don't know if he really purified. I don't
believe so." This should have been both the beginning and the end of HIV.
Retrovirus-like
particles are virtually ubiquitous in biological material,151, 152 including,
for example, cell cultures and "the majority if not all human
placentas".153 (Note that Montagnier refers to EMs obtained from
umbilical-cord blood lymphocytes.) However, as Gallo confirms, the majority of
retrovirus-like particles are not retroviruses because they do not
replicate.151, 154 The "HIV" particle has been "classified"
into two subfamilies and three genera of retroviruses. This is analogous to
describing a new species of mammal as a human, a gorilla and an orang-utan.
Besides the
"HIV" particle, cell cultures contain other particles of numerous
morphologies whose origin and role are unknown.18, 155, 156 A long and detailed
study from Harvard157 revealed the identical "HIV" particle in 18 out
of 20 (90% of) AIDS-related lymph node enlargements but also in 13 out of 15
(88% of) non-AIDS-related enlargements.
HIV experts
claim to detect and even "isolate" HIV merely by demonstrating
"reverse transcription" in cultures. However, although a property of
retroviruses, reverse transcription is not, as many HIV/AIDS experts claim,
unique to retroviruses or even viruses.158, 159 Well before the AIDS era, Gallo
himself showed that chemically stimulated (a technique absolutely essential to
"isolate HIV" from cultures) normal lymphocytes possess this
function.160, 161
The
"HIV" proteins and antibodies
Although both Montagnier and Gallo have never published EMs to prove the presence of
retrovirus-like particles in their "pure virus", and Montagnier now
concedes there weren't any, both groups, and all others since, claim such
material is "pure HIV". This claim is based on the fact that such
material contains proteins which react with antibodies present in AIDS
patients. However, such reasoning is untenable.
Imagine a
scientist who mixes two solutions together, obtains a precipitate and then
proclaims the identity and source of several reactants. One does not need a
degree in chemistry to realise this is an impossibility. Nonetheless, because
cultures and antibodies derived from AIDS patients react together, the proteins
are declared to belong to "HIV" and the antibodies - the
"HIV-specific" antibodies.
In fact, Gallo
admits that, for him, an antibody test is the quintessence of "HIV
isolation". During an interview at the 1998 Geneva AIDS Conference he
admitted: "Sometimes we had Western blot positive but we couldn't isolate
the virus. So we got worried and felt we were getting false positives
sometimes, so we added the Western blot. That's all I can tell you. It was an
experimental tool when we added it, and for us it worked well 'cos we could
isolate the virus when we did it."162 Actually, in 1984, Gallo's
"false positives sometimes" were antibodies in 88% of AIDS patients
but "virus-isolated" in 36% of AIDS patients. Gallo solved the twin
dilemmas of the "missing virus" and gross non-specificity of the
"HIV" antibodies by making the Western blot antibody test an integral
part of virus isolation.
However, an
antibody test is not isolation of a virus. HIV proteins can only be defined by
extracting them from particles purified and proven to be a unique retrovirus.
Such material has never been shown to exist, and such extraction never
reported. Notwithstanding, since the mid-1980s, HIV researchers claim that a
culture which reacts with a monoclonal antibody to one of the "HIV"
proteins, the p24 protein, is proof of isolation of HIV. Since "to isolate
a virus" is to obtain infectious particles separate from everything else,
it is particularly difficult to see how so many scientists persevere in
referring to a chemical reaction in this manner.
The
origin of the "HIV" proteins
According to Eleopulos and her colleagues, all data presented to date are consistent
with the "HIV" proteins being cellular. Using "HIV"
antibodies as probes, "HIV" proteins have been identified in the
tissues of persistently HIV-negative, healthy individuals, including in blood
platelet and skin cells, thymus, tonsil and brain.15 As a mark of the
bewildering status of the HIV theory, while HIV proteins could not be found in
the placentas of 75 HIV-positive, pregnant women,163 they could be found in the
placentas of 25 healthy, HIV-negative women.164
That the HIV
proteins are cellular is further strengthened by a recent two-part experiment.
Human lymphocytes, cultured in the absence of material from AIDS patients, were
"purified" as they would be to obtain the "HIV" proteins.
This "uninfected" material served as a "mock virus" in
experiments involving both "HIV" and "SIV" (simian [monkey]
immunodeficiency virus, claimed similar to "HIV"). Analysis of
"mock virus" reveals qualitatively a series of proteins bearing the
same molecular weights as the proteins of "real" virus, strongly
suggesting that the "HIV" proteins are cellular because the existence
of HIV proteins demands they appear exclusively in cultures derived from AIDS
patients.149
In the second
experiment, monkeys were immunised on several occasions with "mock
virus" - a procedure which subsequently protected them from a
"challenge" with "real" SIV.165, 166 However, immunisation
is specific. Immunisation with hepatitis vaccine does not protect against
poliomyelitis. It relies on exposure of the animal's immune system to material
specific to the organism against which protection is sought. Since proteins
from the cells in which "SIV" is "grown" ("mock"
virus) protect against "real" SIV, these must be exceedingly similar
if not identical. That is, the "SIV" and, by inference, the
"HIV" proteins are all cellular.
The
"HIV genome"
As is the case with the "HIV" proteins, the RNA purported to be the
"HIV" genome has not been obtained from particles purified and proven
infectious, but from the conglomerate material described above. Molecular
biologists have produced possibly more information about the "HIV"
genome than any other object in the Universe. Nonetheless, there are no reports
of even one individual possessing a complete, full-length "HIV"
genome, and there is no agreement as to how many genes HIV possesses. Opinions
have varied from four through to eight, nine or ten. Human DNA and chimpanzee
DNA differ by less than 2%, but variation in the composition of the "HIV
genome" (derived from analysis of "pieces" measuring 2%-30% of
the presumed total) measures between 3%-40%. For comparison, two RNA-containing
viruses (polio and influenza, the latter after 27 years of dormancy) vary by
less than 1%, as do RNA molecules self-assembled in test tubes, denied the
organising influence of living cells.167, 168
Given that the
DNA sequence determines the composition of a virus's proteins, and the latter
the physical, biochemical and biological properties of a virus, how is it
possible for such variation to represent one and the same agent? For example,
how is it possible that HIV can induce the same antibodies which can be recognised
in a universal antibody test containing the identical proteins? Since, as the
molecular biologist Duesberg reminds us, "there is a range, a small range,
in which you can mutate around without too much penalty, but as soon as you
exceed it you are gone, and you are not HIV any longer, or a human any
longer...then you are either dead or you are a monkey, or what have you",8
it is evident that whatever the "HIV DNA genome" represents, it
cannot be a virus.
If there
exists certain RNA which is unique to a retrovirus HIV, then finding such RNA
should prove infection. However, the concordance between antibody and genetic
tests varies between 40%-100%,169 and "HIV" RNA can be found in
individuals not infected with HIV. In responding to this scientific dilemma,
the HIV experts have proclaimed that "Plasma viral load ["HIV"
RNA] assays are designed for monitoring the effectiveness of antiretroviral
therapies and for measuring the quantity of virus in patients with confirmed
HIV infection, not for the diagnosis of HIV infection. Their performance in
patients who are not infected with HIV is unknown" and their use leads to
"Misdiagnosis of HIV infection".170 One manufacturer of PCR states
that "The Amplicor HIV-1 Monitor test is not intended to be used as a
screening test for HIV or as a diagnostic test to confirm the presence of HIV
infection" (Roche Diagnostic Systems, 06/96, 13-08088-001).
These being
the case, the specificity of "plasma viral load" is unknown and it is
difficult if not impossible to claim that "HIV" RNA is the unique
constituent of a specific retrovirus. How can one even consider using such
tests to monitor or diagnose a supposedly deadly virus when the "viral
load" obtained varies between zero and a million copies on the same
sample, depending on which technique or strain of HIV is involved?
Lessons
from the past?
The evidence for the existence of Gallo's "first human" retrovirus (HL23V) was much
stronger than that for HIV (see Part 1).20, 25, 172 However, in 1980, the
antibodies to the HL23V proteins were shown to occur following a large variety
of common, non-infectious factors and in far more humans than could ever have
developed leukaemia.173, 174 Thus, from signifying that an "infectious
mode of transmission [of leukaemia] remains a real possibility in humans"
and "infection with an oncovirus [retrovirus] may be extremely
widespread",175 the "first" human retrovirus abruptly
disappeared from the annals of science. At present no one, not even Gallo,
believes it existed.
However, had
it not been for the efforts of the two research groups at the National Cancer
Institute and Sloan-Kettering, there was the distinct possibility that by now
the world would be facing a pandemic of "HL23V disease" as well as a
pandemic of "HIV disease".
In the AIDS
era, experts recognise that antibodies to the "HIV-specific" proteins
occur where there is no HIV and in many more individuals than will ever develop
AIDS. On what basis, then, does "HIV" still exist?
The DISSIDENT CASE:
POLITICS and PUBLIC HEALTH POLICY
The failures
of the past 15 years are fairly and squarely affixed to the five Montagnier
and Gallo 1983-84 Science papers. That the titles of three of these papers
contain the word "isolation", and yet no such evidence was presented,
must stand as a memorial to the demise of editorial integrity. The dissident
cases - that HIV does not exist (Eleopulos), or, if it does exist, it does not
cause AIDS (Eleopulos/Duesberg) - ultimately imply there will be devastating
outcomes in terms of scientific credibility, including the failure of peer
review, the demise of reputations of many experts and non-experts, the
challenge to citizens' trust in governmental, scientific and medical leaders,
as well as an uncertain period of ignominy for the medical profession as a
whole. Weaving a just resolution through this maze of socio-medico-legal bedlam
will require the utmost perspicacity and tenacity from political leaders.
Perhaps there
are already signs of quiet beginnings with the Americans' 1994 return of the
discovery of HIV to the French, followed by Montagnier's most recent admissions
in his 1997 interview. Perhaps it is also written in the faces of the Nobel
Committee and the stubborn absence of a Nobel Prize awarded for any of the
100,000 scientific papers representing HIV/AIDS research.
Exceptionalism
Over and above all the uncertainties surrounding the HIV/AIDS debate, AIDS
science/medicine must stand as the most remarkable case of
"exceptionalism" in history. The funding it attracts far outstrips
that justified by its prevalence and economic impact.176 For example, over the
past 17 years, Australia has a cumulative total of 7,766 AIDS cases including
5,575 deaths.177, ×××
The big
spenders are (in order) the United States, France, the United Kingdom, Germany and
Italy. Their combined annual HIV/AIDS research budget amounts to US$1.8 billion
for a cumulative total of 761,572 AIDS patients (many of whom are dead). Of an
additional $US20 million spent by the European Union in 1994-98, most
"money goes to support travel and meeting costs rather than laboratory
research".178
While
thousands of dollars per patient are spent on HIV/AIDS research, only a few
dollars are spent on heart disease, cancer, mental illness, suicide prevention
or road trauma.
The funding
paradox reaches epidemic, almost farcical proportions in developing countries
where Western AIDS workers spend their days dispensing advice and condoms to a
population dying for want of potable water, adequate sanitation and nutrition,
and antibacterial, antitubercular and antimalarial medicines - in a word, dying
of poverty.
Currently, the
annual cost of anti-HIV drugs for one person is about $US15,000 (greater than
the entire health budget for many a Third World village). With 650,000 to 900,000
HIV-positive patients in the USA as of July 1996, it would take US$10 billion
to pay for drugs alone. This must be viewed against the World Health
Organization's estimate that by the year 2000 there will be 30 to 40 million
HIV-infected people.
Without HIV,
AIDS patients and specialist AIDS units and their employees can rationally be
absorbed into the existing infrastructure of clinics and hospitals. The pursuit
of expensive drugs designed to kill HIV will be irrelevant, as will be the
travail of the legions of HIV researchers. The same applies to AIDS councils,
the armies of AIDS educators, fundraisers, volunteers and AIDS organisations.
In the US alone, there are 93,000 of the latter - one for every four persons
ever diagnosed with AIDS.34
Clear thinking
Homo sapiens (thinking man) was not named in vain. An honourable society provides
unfettered information and encourages its members to make rational choices.
Epidemi-ology shows that the development of a positive "HIV" antibody
test and AIDS is not so much related to a given sexual practice, but rather to
the frequency of passive anal intercourse in both men and women.
It follows
that AIDS is not a disease of sexual orientation, and as far as women are
concerned it is prudent to note that, in absolute terms, innumerably more women
than men engage in anal intercourse. Thus AIDS is not unlike the case of the
recently appended AIDS-defining disease, cervical cancer, which long before the
AIDS era was known to be related to the frequency of vaginal intercourse. Even
so, it is not the act itself, but the very high frequency of the act, which is
pathogenic.
As serious as
public reaction to an ill-conceived retrovirus may prove, it will not be
anywhere as serious as the legal backlash. There are countless individuals
alive who believe they are infected with a deadly microbe, and many of them are
currently treated with potentially toxic drugs with no proven benefit. They
avoid intimacy, avoid having children, and sometimes avoid even casual contact
with others. It would take a flotilla of poet laureates to voice the collective
pain and suffering engendered by such a mistake. It would take an army of
mathematically gifted lawyers to quantify, and the nation's coffers to
compensate, those whose lives have been ruined by what Neville Hodgkinson has
called "the greatest scientific blunder of the 20th century".29
This is not to
forget patients and relatives who have died at their own hands. In 1987, former
US Senator Lawton Chiles of Florida told an AIDS conference of a tragic case
where 22 blood donors were informed they were HIV-infected on the basis of an
ELISA test. Seven donors then committed suicide.179
In June this
year, the Swiss AIDS analyst Michael Baumgartner persuaded United Nations
officials to include a dissident session at the XIIth International AIDS
Conference held in Geneva. Speakers included: Huw Christie, editor of Continuum
magazine; AIDS analyst and documentary film-maker Joan Shenton; epidemiologist
Professor Gordon Stewart; retrovirologist and electron microscopist Professor
Etienne de Harven; virologist Dr Stefan Lanka; and, by satellite, Eleni
Eleopulos and her group from the Royal Perth Hospital. In the audience were
observers from the Pasteur Institute and the US National Institutes for Health.
The topic of the session was a scientific critique of the HIV antibody tests
and the evidence for the existence of HIV.
At the
official press conference held after the meeting, Professor Bernhard Hirschel,
chairman of the organising committee, accused the speakers of "using
outdated and untrustworthy scientific data". However, it was this
"outdated" data, that of Montagnier and Gallo, that led to the 1984
proclamation that HIV is the cause of AIDS. That considered "untrustworthy"
is the HIV experts' own data.
Notwithstanding
these and many other challenges to the current dogma, HIV/AIDS experts are not
in the least disquieted by sceptical patients, relatives or scientists, and
inveigh heavily against inquisitive journalists alleging great harm to public
health. Thus it appears that the only hope for an immediate resolution of this
troubled issue is to have lawyers appearing for plaintiffs who desire
judgements that they are, or are not, infected with an AIDS-causing virus.
However, even if an examination of "HIV science" is destined to be
scrutinised by courts of law, at present one must be realistic that in the
short term the status quo is extremely unlikely to change.
A real
debate?
Nonetheless, it is inexorably drawing nearer to the time when world governments
will convene an international, adjudicated debate on this subject. In contrast
to the 13,775 participants from 177 countries who attended the June 1998 Geneva
AIDS Conference, this should be a small gathering where a dozen or so experts
from each side put their respective cases to a disinterested group of
scientists of the utmost stature - for example, another dozen made up largely
of Nobel laureates.
There
is a precedent for such a "consensus conference" or conférence de
citoyens in common sense and "along the lines of a model invented in
Scandinavia and since applied in the United Kingdom and elsewhere". A
"jury" of 14 people "screened for independence from interested
parties" would have issues "debated in front of them by scientists,
non-governmental organizations, industrialists and other bodies", as
"The power of public research bodies is probably the best guarantee of
independence with respect to private sector research and the influence of
multinationals".180 By AIDS standards, funding for such a meeting would be
trivial. Indeed, such would be its significance that it would make money for
the organisers.
Perhaps a
disinterested observer could be forgiven for concluding that, although we are
now well into the 18th year of the AIDS era and have spent many billions of
dollars on treatments and research, the words of Dr Peter Duesberg continue to
taunt us: "By any measure, the war on AIDS has been a colossal
failure...our leading scientists and policymakers cannot demonstrate that their
efforts have saved a single life."1
Perhaps the
words of Eleopulos's group are of even greater portent: "The single most
important obstacle in finding the explanation for AIDS is the belief in
HIV."19, 26
In his recent
book, Dancing Naked in the Mind Field, Dr Kary Mullis writes: "Years from
now, people will find our acceptance of the HIV theory of AIDS as silly as we
find those who excommunicated Galileo."2
Indeed, it was
Galileo who counselled: "In Science, the authority embodied in the opinion
of thousands is not worth a spark of reason on one man."
Perhaps,
seventeen years in, we should all pause, look around, and then take a long look
back.
Endnotes:
* US
journalist Christine Johnson's interview (now available in six languages) with
the leader of the Perth group was reviewed by scholar and international gay
media personality Professor Camille Paglia in her column in the US Salon
magazine (28 October 1997): "For a superb critique of the scandalously
overpoliticized scientific research on AIDS, see Christine Johnson's long
interview with Australian biophysicist Eleni Papadopulos-Eleopulos in the new
issue of the British AIDS magazine, Continuum [vol. 5, no. 1, autumn 1997]. The
American major media have effectively suppressed longstanding questions about
whether the AIDS test is reliable or whether an HIV virus in fact exists at
all."
** On 5 May
1998, two US Republicans said they were exploring ways to give a comfortable
retirement to 1,500 chimpanzees that were bred for AIDS research. Accompanied
by primate expert Jane Goodall, House Speaker Newt Gingrich and Rep. Jim
Greenwood (R-Penn.) said they were working on a bill to set up sanctuaries for
the chimps. The chimps, bred in the United States specifically for AIDS
research, did not turn out to be the effective models that scientists had
anticipated. With no research use, the primates that are man's closest cousins
are languishing in cages at an annual cost of US$7.3 million.
*** In 1988,
Eleopulos' paper that HIV does not cause Kaposi's sarcoma was thrice rejected
by the Medical Journal of Australia on the advice of an "established
expert". The reviewer stated: "The author tries to argue that
Kaposi's sarcoma cannot be caused by HIV infection, and that therefore AIDS is
not due to HIV infection. The arguments put forward by the author are quite
unsatisfactory, and are not supported by even a desultory reading of the
literature quoted. In addition, the author fails to examine the body of
epidemiological, immunological and cellular literature concerning the
pathology, pathogenesis and clinical associations of this fascinating
manifestation of HIV infection." Yet this is the very
"epidemiological, immunological and cellular literature" which
eventually led the "established experts" to accept that "this
fascinating manifestation of HIV infection" is not caused by HIV
infection.
× In most
countries, including Australia, individuals with two positive ELISAs have HIV
infection "confirmed" by performing a Western blot test. However,
this testing algorithm selects individuals who have a higher rate of
cross-reacting antibodies and are therefore more likely to react in the Western
blot test. (This is analogous to determining the number of heart attacks in the
community by performing ECGs only on patients with chest pain - an experiment
which grossly underestimates the real number because many heart attacks are
"silent".) On the other hand, England and Wales do not use the HIV WB
to "confirm" reactive HIV ELISAs because Dr Philip Mortimer, Director
of the UK Public Health Laboratory Service, claims that "truly
positive" antibodies are "easily" detected "because these
are reactive in all ["methodologically different machine-read" ELISA]
assays".181 (This reasoning is analogous to performing a chest X-ray with
several machines and claiming a suspicious abnormality is lung cancer because
the appearances are repeatedly the same.) Asked at the 1998 Geneva AIDS
Conference to comment on the UK dropping the Western blot test, Gallo remarked:
"Well, the bulk of the world uses it. If some technology comes across
better, I'd be the first to say 'do it'. I mean, obviously, the Western blot's
a valuable test as defining the proteins that you have antibodies to. Everybody
uses it experimentally and most people use it around the world... Britain
doesn't use it. Maybe there are two countries that have found a better way. God
bless them. Okay?"
×× In
1997, the Perth group attempted a second time to engage the Royal Australasian
College of Surgeons (RACS) in debating the HIV/AIDS controversy by submitting a
paper entitled "A critical analysis of the evidence for the isolation of
HIV" (see website <www.virusmyth.com/aids/data/epappraisal.htm>).
It is RACS editorial policy to "welcome personal views of surgeons on a
variety of topics" and to publish papers on "current and
controversial issues". Although both reviewers accepted the bulk of the
scientific arguments and found the paper "interesting reading", they
advised against publication because, in their view, an analysis of evidence for
the isolation of HIV was of "no real relevance...to a surgical audience"
or "would be of little interest or use to the majority of readers of the
Australian and New Zealand Journal of Surgery".
×××
Of the cumulative 7,766 Australian AIDS cases to date, 387 (5%) are reported in
the "Heterosexual contact" exposure category. However, 22 of these
qualify on the basis of "Sex with injecting drug user", "Sex
with bisexual male", "From high prevalence country" (where
heterosexual spread is deemed dominant), "Sex with HIV-infected person,
exposure not specified", or "Not further specified".177 Thus,
injecting drug use, anal intercourse in women, the presumption of any form of
sexual intercourse, and lack of sufficient data, question the mode of acquiring
HIV infection in at least 330 (85% of) individuals listed in this exposure
category.
×××
Of the cumulative 7,766 Australian AIDS cases to date, 387 (5%) are reported in
the "Heterosexual contact" exposure category. However, 22 of these
qualify on the basis of "Sex with injecting drug user", "Sex
with bisexual male", "From high prevalence country" (where
heterosexual spread is deemed dominant), "Sex with HIV-infected person,
exposure not specified", or "Not further specified".177 Thus,
injecting drug use, anal intercourse in women, the presumption of any form of
sexual intercourse, and lack of sufficient data question the mode of acquiring
HIV infection in at least 330 (85% of) individuals listed in this exposure
category.
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Acknowledgement:
The authors gratefully acknowledge the assistance of Mr Peter Bloch, of General
Media International, and Penthouse Magazine, New York City, for making
available excerpts of Dr Mullis's forthcoming book.
About the Authors:
Valendar F. Turner is a Consultant Emergency
Physician. He can be contacted at the Department of Emergency Medicine, Royal
Perth Hospital, Perth, Western Australia, telephone +61 (0)8 9224 2662, fax +61
(0)8 9224 7045, e-mail <vturner@cyllene.uwa.edu.au>,
website <www.virusmyth.com/aids/perthgroup/>.
Andrew McIntyre is a Melbourne-based
freelance writer and social commentator. He has written extensively on the
gender wars, and takes a particular interest in social and scientific issues
normally avoided or distorted by the mainstream press for reasons of political
expediency or cultural orthodoxy. He appears from time to time on radio and
television. He can be contacted care of NEXUS.
Extracted from
Nexus Magazine, Volume 6,
Number 4 (June-July 1999). And Volume 6,
Number 5 (August-September 1999). And Volume 6,
Number 6 (October-November 1999).
PO Box 30, Mapleton Qld 4560 Australia. editor@nexusmagazine.com
Telephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381
From our web page at: www.nexusmagazine.com
© 1999 by
Valendar F. Turner
Department of Emergency Medicine
Royal Perth Hospital
Perth, Western Australia
telephone +61 (0)8 9224 2662
fax +61 (0)8 9224 7045
e-mail vturner@cyllene.uwa.edu.au
website www.virusmyth.com/aids/perthgroup/
and Andrew
McIntyre
Freelance Journalist
Melbourne, Victoria, Australia
via
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There is a
close connection between the rise of genetic engineering and mixing of viruses in the early 1970s
and the outbreak of HIV in the late 1970s. This connection persists in the form
of the many unprecedented “emerging diseases” caused by “new viruses” that
continue up to the present time.
