A Great Future Behind It

The Yin and Yang of HIV

By Valendar Turner & Andrew McIntyre

Published over three issue of NEXUS Magazine beginning January 1999

SUMMARY

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 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 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 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.
-- Stephen Hawking

A BRIEF HISTORY

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 Kaposis' 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 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) "Non-specific urethritis, hepatitis A, more NSU and gonorrhoea, amoebas [intestinal parasites]-and hepatitis B, more NSU and gonorrhoea, more amoebas, shigella, non-A, non-B hepatitis, giardia, anal fissures, syphilis, more gonorrhoea [penile, anal and oral], gonorrhoea, shigella twice, more amoebas, herpes simplex types I and II; venereal warts, salmonella; chlamydia; cytomegalovirus (CMV); Epstein-Barr virus (EBV); mononucleosis and 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 1120 sex partners.(30) As Callen himself put it, "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. What was "new" was their exponentially escalating prevalence in gay men.

 

Technology and 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 as 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 is still 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 and 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 of Paris published a paper in Science entitled, "Isolation of a T-Lymphotrophic Retrovirus from a patient at Risk for Acquired Immune Deficiency Syndrome (AIDS).(64) It is important to note that the first word in this paper, ‘Isolation’, serves as a signal that the researcher is 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 these "could be used for biomedical, biological and molecular biological studies".(65) 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 (66-69) published four papers also in Science. On the 23rd of April 1984, at a Washington press conference held two weeks before the papers were published, Margaret Heckler, Secretary for Health and Human Services, 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 of Gallo’s 72 (36%) AIDS patients, or barely a third. (The frequency of "isolation" is no better today.(70)).

In 1985 the Pasteur Institute alleged that Gallo had misappropriated their virus. The ensuing conflict, which eventually reached the American 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 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 that Gallo, as laboratory chief, "created and fostered conditions that give rise to falsified/ fabricated data and falsified reports". The final draft report of the OSI, 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. However, despite the long and costly investigation, the OSI concluded that Gallo's research "does not negate the central findings of the [1984] Science paper". 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 their proof that HIV causes AIDS.(16,21)

 

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 Berkeley, California, 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 $US350,000 "outstanding investigator" award from the NIH. But Duesberg dropped a bombshell. He asserted that, apart from the relative 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 1-2 days, the amount of T4 cells needing replacing 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 immune 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 nineteenth century bacteriologist Robert Koch had developed to prove a microbe causes a disease. These four postulates are one, that the organism must be present in all cases of the disease; two, that it must be grown and then isolated in pure culture from the cells of individuals with the disease; three, that it must reproduce the disease when introduced into a susceptible host or experimental animals and four, that from whence it must once again be recovered.

According to Duesberg "From every angle, HIV fails Koch’s first postulate".(1) 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 (12,14,15,71,72) (One percent of human DNA, that is, an amount 3000 times larger than "HIV" DNA, is made up of endogenous retroviral DNA(73)). The third postulate failed because, "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 have 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" compound zidovudine (AZT). In other words, a specific treatment for HIV infection was a cause of AIDS. Duesberg continued to regard HIV bona fide but an inert, harmless "passenger" virus linked to AIDS only through the kinds of activity associated with drug taking (including 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% of HIV positive blood transfusion recipients develop AIDS within one year (but so do 50% of HIV negatives) compared to 1% of haemophiliacs. Kaposis’ sarcoma was to all intents and purposes, confined to gay men.(5,13,74)). 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 Eleopulos' and Duesberg's minds, not a factor. Apparently the role of HIV was also a problem for Montagnier. Although he wrote in Nature in December 1984, "all available data are consistent with the virus being the causative agent of AIDS",(75) 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",(76) 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 Tahi (61) (see below), fuels such speculation.

 

Eleni Papadopulos-Eleopulos and the Perth group

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 she had formulated in the 1970s as a basis for unraveling the genesis and improving the treatment of cancer, and to offer fresh insights into the pathogenesis of cardiovascular diseases and aging. Eleopulos postulates that normal cellular functioning is determined by the level and oscillations of cellular redox (23) (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 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 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 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.(11,24,63,77)

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, Kaposis’ 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.(12,13,54,74,78 §) In the OECD countries the prediction of a sexual pandemic fails completely. For example, as of the beginning of 1998, 93% 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, beriberi and scurvy which also remain confined to their risk groups. All are caused by vitamin deficiencies but in the past were regarded infectious and sufferers 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 before the turn of the century 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 of passive anal intercourse in both sexes, HIV positive and AIDS patients being oxidised relative to normal individuals, the ameriolation of HIV/AIDS by the use of antioxidants and a non-infectious animal model. Everyone of these predictions has materialised. Oxidative stress is well established by hundreds of papers,(14,62,79-81) so much so that in the early 1990s the Pasteur Institute was advertising international scholarships to study the phenomenon. In fact this year Luc Montagnier is the principal editor of a 558 page book devoted to oxidative stress in cancer, aging and AIDS.(82)

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 T4 cells "disappear" regardless of whether one adds "HIV" or merely the chemical stimulants obligatory to "grow" the "HIV".(83) 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 Disease (84) and Dr. Zvi Grossman at the University of Tel Aviv.85

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 numbers 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 noninfectious virus" or virus or "rendered defective" by "anti-HIV" drugs, could still contribute to the loss of T4 cells throughout the course of HIV disease.(86) In other words, "alive" or "dead", HIV causes immune deficiency. Such a proposal does not auger well for the use or continued development of "anti-HIV" drugs.

Consistent also with the Eleopulos oxidatives 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, Kaposi's sarcoma-like tumors and "abundant" retroviral-like particles appear in their spleens.(87) Thus AIDS diseases are followed by the production of retroviral-like particles and not the other way around.

 

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, individuals whose only motivation is to contribute to solving a disease claimed to afflict millions of people, find themselves censored. For example, the editor of the world’s most prestigious 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 any scientific reasons and invariably citing space constraints in the journal. Professor John Kaldor, one of Australia's foremost "established experts" on AIDS admits that dissidents "intersperse their cases with grains of fact".(88) 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.

 

The rise and fall of the "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) In 1994, a double-blind randomised comparison of two policies of AZT treatment (immediate and deferred) was reported (the Concorde trial). This involved 1749 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".(89) In 1995, extended results of Concorde showed a significant increased risk of death among the patients treated early. However, despite these data, disclaimers that patients treated with AZT may continue to develop the AIDS diseases, that the side effects of AZT may mimic AIDS, and AZT given to non-HIV-infected babies causes the AIDS defining pneumonia PCP,(90) 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 antiretrovirals... I've been following them since the very beginning...They've watched all of their friends go on the antiviral bandwagon and die".(91) Indeed, even an elementary study of the relevant pharmacologicaL literature reveals that AZT cannot be an anti-HIV drug.(92)

In 1996, the latest drugs, the "protease inhibitors" (PI) were introduced. These are prescribed as one of up to 200 possible "cocktails" with AZT or similar drugs. Detailed data on these drugs of the kind usually reserved for medical practitioners, appear regularly in glossy, multi-page advertisements in gay mens’ magazines. At the July 1996 XIth 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".(93) At the July 1998 XIIth AIDS conference Ho stated it will take at least ten years of intense combination drug therapy to kill off all the HIV in an infected person's body but a sizable 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.(94-97) 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 writes, "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".(85)

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 NIH. "Trying to rid the body of a virus whose genome is incorporated into the host genome may be impossible".(98) Indeed, how can a drug rid a body of material so intimately bound to the host DNA genetic material?

 

SOME SCIENTIFIC PROBLEMS WITH THE HIV THEORY

 

The theory versus 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, 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 AIDS if he or she fulfills the criteria set out in the latest (1993) revision of the US "CDC surveillance case definition for AIDS".(99) (Other definitions in use around the world make scientific comparisons almost impossible. In Africa AIDS is diagnosed on symptoms and without blood tests (100)). Since from 1985 the CDC "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 Kaposis’ sarcoma which even Gallo (54) 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"(101) (italics ours).

 

Sexual transmission

HIV/AIDS is claimed to be bidirectionally sexually transmitted. Data to support this claim is based not upon microbial isolation and contact tracing as is the orthodox practice for proving diseases are infectious and sexually transmitted (STD), but on mostly retrospective studies of highly selected groups of individuals including gay and bisexual men, heterosexual men and women including prostitutes, for antibodies in blood which react 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.

 

Gay 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" (102). They also found the more often a gay man has 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 gay men.(103) In an extensive review of 25 studies of gay 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".(104) In the West, the largest and most judiciously conducted prospective epidemiological studies such as the Multicenter AIDS Cohort Study (MACS) of 4955 gay men (105) have proven beyond all reasonable doubt that in gay 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 gay 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, although the Royal Australasian College of Surgeons considers HIV positive surgeons "to be infectious and should not perform invasive procedures or operations. However, "(t)hey may provide these services to patients who have the same infection".(106)

 

Heterosexuals

The largest and best conducted studies in heterosexuals including the European Study Group (107) show 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 ten year study of heterosexual couples (1986-1996).(108) There were two parts to this study, one cross-sectional, the other prospective. In the former "The constant per-contact infectivity for male-to-female transmission was estimated to be 0.0009 [1/1111]". The risk factors for the women were: (i) anal intercourse;. (ii) having partners who acquired this infection through drug use (Padian says that 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 positive female cases only 2 became HIV positive but under circumstances considered ambiguous by Padian. In the prospective study, starting in 1990, 175 HIV-discordant couples were followed for approximately 282 couple-years. At entry, one third used condoms consistently and in the six months prior their last follow up visit, 26% of couples consistently failed to use condoms. There were no seroconversions after entry including the 47 couples not using condoms consistently. Based on the 2/86 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 1/9000 per contact. From this statistic one can calculate that on average, a male would need to have 6000 sexual contacts with an infected female to achieve a 50% chance of becoming HIV positive. At three contacts per week this would take 56 years, or a life time.

 

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, as it is widely accepted, 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, given the facts that prostitutes are frequented by bisexual men and, 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 were positive.(109)

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 20. None were positive.(110)

In 1985, 132 prostitutes (and 55 non-prostitutes) who attended a Sydney STD clinic were tested for HIV antibodies. The average numbers 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 (11%) of prostitutes used condoms at all and 49% of their partners used condoms in fewer than 20% of encounters. No women were positive.(111)

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 percent 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 positive.

At the time of this report, a decade into the AIDS era, the authors also commented, "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 "there are still many women working as prostitutes in Sydney who remain seriously at risk of HIV infection".(112) In Spain, of 519 non-IVDU prostitutes tested between May 1989 and December 1990, only 12 (2.3 per cent) had positive test, which was "only slightly higher than that reported 5 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, "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".(113)

Similar data from two Scottish studies,(114) the 1993 "European working group on HIV infection in female prostitutes study",(115) and a 1994 report of 53,903 Filipino prostitutes tested between 1985 to 1992, confirm that non-IVDU prostitutes remain virtually devoid of HIV infection. For example, in the latter study, only 72 (0.01%) women were found to be HIV positive.

In studies where there appear 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.(116) 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 5674 (44%) and 4360 (34%) of the 12785 Cambodian "HIV and AIDS Case Reports" till 31/12/97 are listed as "Unknown" gender and age respectively,(117) data collection, at least by the WHO 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 heterosexual activity without condoms), found that no babies or mothers were HIV positive.(118) 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". (Weiss, 1998 #1179) The "overwhelming" evidence from studies both in gay 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 Tubingen, 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 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 Western blot, "HIV" proteins are first separated along the length of a nitrocellulose strip. This enables individual reactions to the ten 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,(119,120) 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 infected with HIV. (Notwithstanding, in the MACS, one band remained proof of HIV infection in gay men until 1990 (121)). On the other hand, although AIDS began to decline in 1987,(122,123) this trend was countered by the addition of more and more diseases and, most recently, mere laboratory abnormalities to each revision (1985, 1987 and 1993) of the first, 1982 CDC definition. The net effect of these changes was to maintain the 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, for example, (a) amongst 89,547 anonymously tested blood specimens from 26 US hospital patients at no risk of AIDS, between 0.7% to 21.7% of men and 0-7.8% of women aged 25-44 years were found to be HIV WB positive.(124) (It is estimated that approximately 1% of men are gay. 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). (b) the US Consortium for Retrovirus Serology Standardization reported that 127/1306 (10%) of 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 (119) (see below). Thus the correlation between "HIV" antibodies and AIDS, which experts accept as the only proof that HIV causes AIDS, could not be a statistic related to the natural, unbridled activity of a virus but is instead a contrivance of mankind. Not only does correlation never prove causation, the artificiality of this particular "correlation" disqualifies it from meaningful 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 (Figure 1). The global variation in interpretive criteria means for example, that in Australia 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 elswhere. A virus cannot behave in this manner, but, according to the HIV test, which is claimed to have a specificity of 99.999%,(125) 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 HIV infected.(101). 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 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 protein bands and is common"(120) (20-25%). However Eleopulos argues, 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 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, Dr. Elizabeth Dax, the head of the NRL was asked to justify both the Australian criteria for a positive Western blot and the global variability.(28) Her response (126) avoided answering either question and subsequent correspondence failed to pass the editorial staff at the Medical Journal of Australia. When the same questions were later put via the Offices of Senator Chris Ellison, Minister for Schools, Vocational Education and Training, 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".(120)

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 being in widespread use and "a stalwart" (126) of HIV testing, these data have never been reported. This is an issue the NRL chronically and negligently fails to address. 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; (b) unlike Australians, Africans, (similar to the AIDS risk groups), are exposed to a multitude of infectious agents producing a myriad of antibodies each capable of cross-reactions; "false reactivity" will be much higher in Africa where the WB criteria should be the most stringent. Indeed, if it is true that "HIV" antibodies prove one third of heterosexual adults in certain central and east 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 are unique constituents of an exogenous retrovirus, and if such a virus induces specific antibodies, we would never expect to find "HIV" antibodies in the absence of HIV. Yet, in addition to the circumstances above, there are numerous others where antibodies to the "HIV specific" proteins arise where HIV/AIDS experts concede there is no HIV. These include healthy mice injected with lymphocytes of similar mice (127) or bacterial extracts;(V. Colizzi et al., personal communication), following transfusions of HIV free blood (128) or a person's own irradiated blood,(129) and in 72/144 dogs tested at a Veterinary clinic in Davis USA.(130) In addition, antibodies to the microbes which cause the fungal and mycobacterial diseases affecting 90% of AIDS patients react with the "HIV specific" proteins.(20,131) 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% of hepatitis C, all non-HIV, non-AIDS diseases, have antibodies to the "HIV" p24 "core" protein;(132)

Until 1990, an unknown number of the 4955 gay 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 rigorous in gay men? 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 woman as "compelling evidence" for transmission of HIV from a gay man during the course of minor, office surgery in 1989.(133) However, there was no proof that the gay 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 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. However, 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,(134) the College accepted these data as proof of cross-infection but concluded "The mode of transmission is unknown".(106 §§)

 

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 that makes DNA from RNA (reverse transcription); 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,(135,136) it has been ignored by all HIV researchers.

Although there are electron microscope (EM) pictures from unpurified cell cultures of particles purported to be "HIV", it was not until March 1997 that EMs of "purified HIV" were published.(137,138) 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 pictures 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 which "copurify" (sic) with the cellular material. Close examination of these particles as well as other evidence in the papers show they are too large, wrongly shaped, have too high a mass and are devoid of knobs HIV experts unanimously assert are absolutely essential for the "HIV" particle to cause infection. It is from this material, 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 July 17th 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. They were very different. Relatively different. So with the [unpurified] cultures it took many hours to find the first pictures. It was a Roman effort!… Charles Dauget [an EM expert] looked at the plasma, the concentrate, etc… he saw nothing major"(61) ( italics ours). Questioned about the Gallo group he 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.

Retroviral-like particles are virtually ubiquitous in biological material (139,140) including for example cell cultures and "in the majority if not all, human placentas".(141) (One should note that Montagnier’s "Roman effort" refers to EMs obtained from umilical cord blood lymphocytes). However, as Gallo confirms, because they do not replicate, the majority of retroviral-like particles are not retroviruses.(139,142) 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 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.(18,143,144) A detailed study from Harvard (145) revealed the identical "HIV" particle in 18/20 (90%) of AIDS as well as in 13/15 (88%) of non-AIDS related lymph node enlargements.

HIV experts claim to detect and even "isolate" HIV merely by demonstrating "reverse transcription" in cultures. However, although present in retroviruses, reverse transcription is not, as many HIV/AIDS experts claim, unique to retroviruses or even viruses.(146,147) Well before the AIDS era Gallo himself showed that chemically stimulated (absolutely essential to "isolate HIV" from cultures) lymphocytes, possess this function.(148,149)

 

The "HIV" proteins and antibodies

Although both Montagnier and Gallo have never published EMs to prove the presence of retroviral-like particles in their "pure virus", and Montagnier now concedes there were none, 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, this 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 Geneva AIDS conference he said, "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".(150) However, HIV isolation is not an antibody test and "HIV" proteins can only be defined by extracting them from particles purified and proven to be a retrovirus. Such material has never been shown to exist and such extraction never reported. Notwithstanding, since the mid 1980s, HIV researchers claim that the reaction between cell cultures and an antibody to merely one, the p24 protein, is "HIV isolation". Since "to isolate a virus" is to obtain infectious particles separate from everything else, it is particularly difficult to see how scientists can refer to a chemical reaction in this manner.

 

The origin of the "HIV" proteins

According to Eleopulos and her colleagues, all data presented to date is 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 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,(151) they could be found in the placentas of 25 healthy, HIV negative women.(152) 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, is "purified" as it would be to obtain the "HIV" proteins. This "uninfected" material serves 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.(137) In the second experiment, monkeys are immunised on several occasions with "mock virus", a procedure which subsequently protects them from a "challenge" with "real" SIV.(153,154) However, immunisation is specific. Immunisation with hepatitis vaccine does not protect against poliomyelitis. It relies on exposure of the animal to material specific to the organism against which protection is sought resulting in the production of specific antibodies by the immune system. Since proteins from the cells in which "SIV" is "grown" ("mock" virus), protects 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. Man and chimpanzee DNA differ by less than 2% but variation in the composition of the "HIV genome" (derived from analysis of "pieces" measuring 2% to 30% of the presumed total) measures between 3-40%. By 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.(155,156)

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 and 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.

 

Lessons from the past?

The evidence for the existence of Gallo’s "first human" retrovirus (HL23V) was much stronger than that for HIV.(20,25,157) 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 have ever developed leukaemia.(158,159) 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",(160) the "first" human retrovirus abruptly disappeared from the annals of science. At present no one, not even Gallo, believes it existed. 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 fifteen 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 does not cause AIDS (Eleopulos and Duesberg), ultimately implies there will be devastating outcomes in terms of scientific credibility including the failure of peer review, the reputations of many experts and non-experts, a challenge to the trust the citizen places in the hands of government, 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 1994 return of the discovery of HIV to the French by the Americans followed by the most recent admissions of Montagnier 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 and 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.(161) For example, over the past 17 years Australia has a cumulative total of 7,766 cases of AIDS including 5575 deaths.(162 ¥§) 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".(163) 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, antibacterial, antitubercular and antimalarial medicines. In a word, dying of poverty.

Currently, the annual cost of anti-HIV drugs for one person costs about $US15,000 (which is greater than the entire health budget for many a third world village). With 650,000 to 900,000 HIV positive patients in the US as of July 1996, it would take $10 billion to pay for drugs alone. This must be viewed against the World Health Organisation's estimate that by the year 2000 there will be 30-40 million HIV infected people. Without HIV, AIDS patients, specialist AIDS units and their employees can rationally be absorbed into 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, AIDS fund raisers, 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. Epidemiology 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. 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 frequencies 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, many of whom are currently treated with potentially toxic drugs with no proven benefit. They avoid intimacy, avoid having children and sometimes 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 who lives have been ruined by what Neville Hodgkinson has called "the greatest scientific blunder of the 20th century".(29) This is not to mention 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 twenty two blood donors were informed they were HIV infected on the basis of an ELISA test. Seven then committed suicide.(164)

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, the 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 from Perth, 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, the "outdated" data is that of Montagnier and Gallo which 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 the only hope for an immediate resolution of this troubled issue is lawyers appearing for plaintiffs desiring 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 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 ‘conference 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" have issues "debated in front of them by scientists, non-governmental organizations, industrialists and other bodies…The power of public research bodies is probably the best guarantee of independence with respect to private sector research and the influence of multinationals".(165) By AIDS standards, funding for such a meeting would be trivial. Indeed, such would be its significance it would make money for the organisers.

Perhaps a disinterested observer could be forgiven for concluding that, although we are approaching the eighteenth year of the AIDS era, and have spent many billions of dollars on treatments and research, the words of 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 those of Eleopulos 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 counseled, "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.

 

Dr. Valendar F. Turner, Department of Emergency Medicine, Royal Perth Hospital, Perth, West Australia. Andrew McIntyre, Freelance Journalist, Melbourne, Victoria, Australia
Voice 08 92242662
Fax 08 92247045
Email vturner@westnet.com.au

Website http://www.theperthgroup.com

 

ACKNOWLEDGEMENT

The authors gratfully acknowledge the assistance of Mr. Peter Bloch of General Media International and Penthouse Magazine New York City for making available excerpts of Dr. Mullis’ forthcoming book.

 

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 October 28th 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. The American major media have effectively suppressed long-standing questions about whether the AIDS test is reliable or whether an HIV virus in fact exists at all".

**On May 5th 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 $US7.3 million.

§ In 1988, Eleopulos' paper that HIV does not cause Kaposis' 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 Kaposis' 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.

¥ Asked to comment at the Geneva conference on the fact that England and Wales have dropped the use of the WB to "confirm" positive HIV ELISAs, Gallo commented, "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. Not in Eng…,Britain doesn’t use it, maybe there are two countries that have found a better way. God bless them. OK?"

§§ In 1997 the Perth group attempted a second time to engage the Royal Australasian College of Surgeons in debating the HIV/AIDS controversy by submitting a paper entitled "A critical analysis of the evidence for the isolation of HIV" (www.virusmyth.com/aids/data/epappraisal.htm). It is 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 7766 Australian AIDS cases, 387 (5%) are reported in the "heterosexual contact" exposure category. However, 22 of these qualify on the basis of "Sex with injecting drug user", 35 "Sex with bisexual male", 56 "From high prevalence country" (where heterosexual spread is deemed dominant), 47 "Sex with HIV-infected person, exposure not specified", 170 "Not further specified". 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.

 

REFERENCES:

1. Duesberg PD. (1996). Inventing the AIDS Virus. Washington, USA: Regnery Publishing, Inc., 1996.

2. Mullis KB. (1998). Dancing Naked in the Mind Field: Pantheon, 1998.

3. Duesberg PH. (1987). Retroviruses as carcinogens and pathogens: Expectations and reality. Cancer Res. 47:1199-1220.

4. Duesberg PH. (1989). Human immunodeficiency virus and acquired immunodeficiency syndrome: correlation but not causation. Proc. Natl. Acad. Sci. U S A 86:755-764.

5. Duesberg PH. (1992). AIDS acquired by drug consumption and other noncontagious risk factors. Pharmacol. Ther. 55:201-277.

6. Duesberg PH. (1995). Foreign-protein-mediated immunodeficiency in hemophiliacs with and without HIV infection. Genetica 95:51-70.

7. Duesberg P, Rasnick D. (1997). The drugs-AIDS hypothesis. Continuum 4:1s-24s.

8. Duesberg PH. (1996). Peter Duesberg responds. Continuum 4:8-9.

9. Papadopulos-Eleopopulos E, Turner VF, Papadimitriou JM, Hedland-Thomas B, Causer D, Page B. (1995). A critical analysis of the HIV-T4-cell-AIDS hypothesis. Genetica 95:5-24.

10. Papadopulos-Eleopopulos E, Turner VF, Papadimitriou JM, Causer D. (1995). Fator VIII, HIV and AIDS in haemophiliacs: an analysis of their relationship. Genetica 95:25-50.

11. Papadopulos-Eleopopulos E, Turner VF, Papadimitriou JM, Bialy H. (1995). AIDS in Africa: Distinguishing fact and fiction. World J. Microbiol. Biotechnol. 11:135-143.

12. Papadopulos-Eleopulos E. (1988). Reappraisal of AIDS: Is the oxidation caused by the risk factors the primary cause? Med. Hypotheses 25:151-162.

13. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1992). Kaposi's sarcoma and HIV. Med. Hypotheses 39:22-9.

14. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1992). Oxidative stress, HIV and AIDS. Res. Immunol. 143:145-8.

15. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1993). Is a positive Western blot proof of HIV infection? Bio/Technology 11:696-707.

16. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1993). Has Gallo proven the role of HIV in AIDS? Emerg. Med. [Australia] 5:113-123.

17. Papadopulos-Eleopulos E, Turner VF, Causer DS, Papadimitriou JM. (1996). HIV transmission by donor semen. Lancet 347:190-1.

18. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. (1996). Virus Challenge. Continuum 4:24-27.

19. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D. (1996). The Isolation of HIV: Has it really been achieved? Continuum 4:1s-24s.

20. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D. (1997). HIV antibodies: Further questions and a plea for clarification. Curr. Med. Res. Opinion 13:627-634.

21. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D. (1997). A critical analysis of the evidence for the isolation of HIV. At website www.virusmyth.com/aids/data/epappraisal.htm .

22. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D. (1995). A reply to Wei and Ho. At website www.virusmyth.com/aids/perthgroup/ .

23. Papadopulos-Eleopulos E. (1982). A Mitotic Theory. J. Theor. Biol. 96:741-758.

24. Papadopulos-Eleopulos E, Turner VF. (1994). Deconstructing AIDS in Africa. The Independent Monthly 50-51.

25. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D, Page B. (1998). HIV Antibody Tests and Viral Load - More Unanswered Questions and a Further Plea for Clarification. Curr. Med. Res. Opinion 14:185-186.

26. Papadopulos-Eleopopulos E, Turner VF, Papadimitriou JM, Causer D. (1997). Why no whole virus? Continuum 4:27-30.

27. de Harven E. (1997). Pioneer deplores "HIV". Continuum 5:24.

28. Turner VF. (1994). The HIV Western blot. Med. J. Aust. 160:807-808.

29. Hodgkinson N. (1996). AIDS The failure of contemporary science. London: Fourth Estate, 1996.

30. Callen M. (1991). Surviving AIDS. Harper Collins: Harper Collins Publishers, 1991.

31. Johnson C. (1997). Is HIV the cause of AIDS? Continuum 5:8-19.

32. De Marchi L, Franchi F. (1996). AIDS la grande truffa. ROME: Edizioni SEAM, 1996.

33. Shenton J. (1998). Positively false. London: I. B. Tauris, 1998.

34. Maggiore C. (1997). What if everything you thought you knew about AIDS was wrong? Los Angeles: HEAL, 1997.

35. McDonald JF, ed. Genetica. London: Kluwer Academic Publishers, 1995.

36. Anonymous. (1995). Missing Virus: The Jody Wells Memorial Prize. Continuum 3:4.

37. Brody S. (1997). Sex at Risk: Lifetime Number of Partners, Frequency of Intercourse, and the Low AIDS Risk of Vaginal Intercourse. New Brunswick NJ: Transaction Publishers, 1997.

38. Caton H. (1994). The AIDS Mirage. Sydney: The University of New South Wales Press Ltd., 1994.

39. Chirimuuta RC, Chirimuuta RJ. (1987). Aids, Africa and Racism. 1st ed. Bretby House Stanhope Bretby, Burton-on-Trent, United Kingdom: R. Chirimuuta, 1987.

40. Christie H. (1995). HIV Positive? It depends where you live. Continuum 3:21.

41. Christie H. (1996). Counterculture. Continuum 4:18-21.

42. Christie H. (1997). From Hype to Hesitation. Continuum 4:11-12.

43. Christie H. (1998). Wake the law. Continuum 5:28-29.

44. Christie H. (1998). Do antibody tests prove HIV infection? Continuum 5:10-19.

45. Cohen J. (1994). The Duesberg Phenomenon. Science 266:1642-1649.

46. Current S. (1995). HIV and AIDS: Causation or coercion? Provincetown Positive 19-22.

47. Gildemeister V. (1996). Is Maddox mad or is he just pretending? Continuum 4:6-7.

48. Hodgkinson N. Research disputes epidemic of Aids. Sunday Times 1994 22nd May;24.

49. Hodgkinson N. World AIDS Conference. The European 1998 ;30.

50. Konotey-Ahulu. (1987). AIDS in Africa: Misinformation and Disinformation. Lancet ii:206-207.

51. Koliadin VL. (1995). Critical analysis of the current views on the nature of AIDS. Genetica 95:71-90.

52. Koliadin VL. Some facts behind the expansion of the definition of AIDS in 1993: Personal Communication, 1997.

53. Lauritsen J. (1993). The AIDS War. New York City: Asklepois Press, 1993.

54. Lauritsen J. (1994). Gallo admits...we have never found HIV DNA in Kaposi's sarcoma. Continuum 2:4.

55. Lauritsen J. (1994). NIDA Meeting Calls for Research into the Poppers-Kaposi's Sarcoma Connection. The New York Native At website www.virusmyth.com/aids/data/jlpoppers.htm.

56. Lauritsen J. (1990). Poison by prescription--The AZT story. New York: Asklepois Press, 1990.

57. Padian N, Pickering J. (1986). Female-to-male transmission of AIDS: a reexamination of the African sex ratio of cases. JAMA 256:590.

58. Root-Bernstein RS. (1993). Rethinking AIDS-The tragic cost of premature consensus. New York: Macmillan, Inc., 1993.

59. Root-Bernstein RS. (1995). Five myths about AIDS that have miscredited research and treatment. Genetica 95:111-132.

60. Mullis KB. (1995). A hypothetical disease of the immune system that may bear some relation to the Acquired Immune Deficiency Syndrome. Genetica 95:195-197.

61. Tahi D. (1998). Did Luc Montagnier discover HIV? Text of video interview with Professor Luc Montagnier at the Pasteur Institute July 18th 1997. Continuum 5:30-34.

62. Turner VF. (1990). Reducing agents and AIDS--Why are we waiting? Med. J. Aust. 153:502.

63. Turner VF. (1998). Where we have gone wrong? Continuum 5:38-44.

64. Barré-Sinoussi F, Chermann JC, Rey F, et al. (1983). Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS). Science 220:868-71.

65. Gallo RC, Sarin PS, Kramarsky B, Salahuddin Z, Markham P, Popovic M. (1986). First isolation of HTLV-III. Nature 321:119.

66. Gallo RC, Sarin PS, Gelmann EP. (1983). Isolation of Human T-Cell Leukemia Virus in Acquired Immune Deficiency Syndrome (AIDS). Science 220:865-867.

67. Popovic M, Sarngadharan MG, Read E, Gallo RC. (1984). Detection, Isolation,and Continuous Production of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and Pre-AIDS. Science 224:497-500.

68. Sarngadharan M, G., Popovic M, Bruch L. (1984). Antibodies Reactive to Human T-Lymphotrophic Retroviruses (HTLV-III) in the Serum of Patients with AIDS. Science 224:506-508.

69. Schupbach J, Popovic M, Gilden RV, Gonda MA, Sarngadharan MG, Gallo RC. (1984). Serological analysis of a Subgroup of Human T-Lymphotrophic Retroviruses (HTLV-III) Associated with AIDS. Science 224:503-505.

70. WHO. (1994). HIV type 1 variation in World Health Organization-sponsored vaccine evaluation sites: genetic screening, sequence analysis, and preliminary biological characterization of selected viral strains. AIDS Res. Hum. Retroviruses 10:1327-1343.

71. Temin HM. (1974). On the origin of RNA tumor viruses. Harvey Lect. 69:173-197.

72. Weiss RA, Friis RR, Katz E, Vogt PK. (1971). Induction of avian tumor viruses in normal cells by physical and chemical carcinogens. Virol. 46:920-938.

73. Lower R, Lower J, Kurth R. (1996). The viruses in all of us: Characteristics and biological significance of human endogenous retrovirus sequences. Proc. Natl. Acad. Sci. U S A 93:5177-5184.

74. Beral VD, Bull R, Darby S. (1990). Kaposis sarcoma and sexual practices associated with faecal contact in homosexual or bisexual men with AIDS. Lancet 339:632-636.

75. Alizon M, Sonigo P, Barre-Sinoussi P, et al. (1984). Molecular cloning of lymphadenopathy-associated virus. Nature 312:757-760.

76. Montagnier L. (1985). Lymphadenopathy-Associated Virus: From Molecular Biology to Pathogenicity. Ann. Int. Med. 103:689-693.

77. Papadopulos-Eleopulos E, Turner VF. (1995). Reconstructing AIDS in Africa-Reply to Kaldor and Ashton. The Independent Monthly Feburary:23-24.

78. Beral V, Peterman TA, Berkelman RL, Jaffe HW. (1990). Kaposi's sarcoma among persons with AIDS:a sexually transmitted infection? Lancet 335:123-128.

79. Buhl R, Jaffe HA, Holroyd KJ, et al. (1989). Systemic glutathione deficiency in symptom-free HIV-seropositive individuals. Lancet 2:1294-8.

80. Eck HP, Gmunder H, Hartmann M, Petzoldt D, Daniel V, Droge W. (1989). Low concentrations of acid-soluble thiol (cysteine) in the blood plasma of HIV-1-infected patients. Biol. Chem. Hoppe-Seyler 370:101-8.

81. Herzenberg LA, De Rosa SC, Dubs JG, et al. (1997). Glutathione deficiency is associated with impaired survival in HIV disease. Proc. Natl. Acad. Sci. U S A 94:1967-72.

82. Montagnier L, Olivier R, Pasquier C, eds. Oxidative stress in cancer, AIDS and neurogenerative diseases. New York: Marcel Dekker Inc, 1998.

83. Zagury D, Bernard J, Leonard R, et al. (1986). Long-Term Cultures of HTLV-III-Infected T Cells: A Model of Cytopathology of T-Cell Depletion in AIDS. Science 231:850-853.

84. Rosenberg YJ, Anderson AO, Pabst R. (1998). HIV-induced decline in blood CD4/CD8 ratios: viral killing or altered lymphocyte trafficking? Immunol. Today 19:10-7.

85. Grossman Z, Feinberg MB, Paul WE. (1998). Multiple modes of cellular activation and virus transmission in HIV infection: A role for chronically and latently infected cells in sustaining viral replication. Proc. Natl. Acad. Sci. U S A 95:6314-6319.

86. Poon B, Grovit-Ferbas K, Stewart SA, Chen ISY. (1998). Cell cycle arrest by vpr in HIV-1 virions and insensitivity to antiretroviral agents. Science 281:266-269.

87. Ter-Grigorov VS, Krifuks O, Liubashevsky E, Nyska A, Trainin Z, Toder V. (1997). A new transmissible AIDS-like disease in mice induced by alloimmune stimuli. Nat. Med. 3:37-41.

88. Kaldor J, Ashton L. (1995). The AIDS debate: Reconstructing AIDS in Africa. The Independent Monthly 23-24.

89. Anonymous. (1994). Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and deferred zidovudine in symptom-free HIV infection. Concorde Coordinating Committee. Lancet 343:871-81.

90. Heresi GP, Caceres E, Atkins JT, Reuben J, Doyle M. (1997). Pneumocystis carinii pneumonia in infants who were exposed to human immunodeficiency virus but were not infected: an exception to the AIDS surveillance case definition. Clin. Infect. Dis. 25:739-40.

91. Abrams D. Lecture to Medical Students. Synapse, 1996.

92. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D, Miller T, Alphonso H. (1999). A critical analysis of the pharmacology of AZT and its use in AIDS. Curr. Med. Res. Opinion in press.

93. Kilzer L. Optimistic AIDS reports beguiling at risk men. The Rocky Mountain News 1998 May 3rd;3A.

94. O. Brien W, Grovit-Ferbas K, Namazi A, et al. (1995). Human immunodeficiency virus-type 1 replication can be increased in peripheral blood of seropositive patients after influenza vaccination. Blood 86:1082-9.

95. Lee TH, Sheppard HW, Reis M, Dondero D, Osmond D, Busch MP. (1994). Circulating HIV-1-infected cell burden from seroconversion to AIDS: importance of posseroconversion viral load on disease course. J. Acquir. Immun. Defic. Syndr. 7:381-388.

96. Holodniy M, Mole L, Winters M, Merigan TC. (1994). Diurnal and short-term stability of HIV virus load as measured by gene amplification. J. Acquir. Immun. Defic. Syndr. 7:363-8.

97. Bruisten SM, Reiss P, Loeliger AE, et al. (1998). Cellular proviral HIV type 1 DNA load persists after long-term RT-inhibitor therapy in HIV type 1 infected persons. AIDS Res. Hum. Retroviruses 14:1053-1058.

98. Garrett L. AIDS, After The `Cure' / Amid setbacks, search for new hope. Newsday, Sunday 1998 June 14th;A07.

99. CDC. (1992). 1993 Revised Classification System for HIV Infection and Expanded Surveillance Case Definition for AIDS Among Adolescents and Adults. MMWR 41:1-19.

100. WHO. (1986). Acquired Immunodeficiency Syndrome (AIDS) WHO/CDC case definition for AIDS. Wkly. Epidem. Rec. 61:69-76.

101. Fauci AS, Lane HC. Human Immunodeficiency Virus (HIV) Disease: AIDS and Related Disorders. (1994). p. 1566-1618 In: Harrison's Principles of Internal Medicine Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper DL, eds 13th ed McGraw-Hill Inc., New York.

102. Goedert JJ, Sarngadharan MG, Biggar RJ, et al. (1984). Determinants of retrovirus (HTLV-III) antibody and immunodeficiency conditions in homosexual men. Lancet 2:711-6.

103. Stevens CE, Taylor PE, Zang EA, et al. (1986). Human T-cell lymphotropic virus type III infection in a cohort of homosexual men in New York City. JAMA 255:2167-2172.

104. Caceres CF, van Griensven GJP. (1994). Male homosexual transmission of HIV-1. AIDS 8:1051-1061.

105. Kingsley LA, Kaslow R, Rinaldo CR, et al. (1987). Risk factors for seroconversion to human immunodeficiency virus among male homosexuals. Lancet i:345-348.

106. West RH, O'Connor TW, Penny R, et al. (1998). Policy Document Infection Control in Surgery. Melbourne: Royal Australasian College of Surgeons, 1998.

107. European Study Group. (1989). Risk factors for male to female transmission of HIV. Brit. Med. J. 298:411-414.

108. Padian NS, Shiboski SC, Glass SO, Vittinghoff E. (1997). Heterosexual transmission of human immunodeficiency virus (HIV) in northern California: results from a ten-year study. Am. J. Epidemiol. 146:350-357.

109. Anonymous. (1985). HTLV-III antibody in prostitutes. Lancet ii:1424.

110. Krogsgaard K, Gluud C, Pederson C, et al. (1986). Widespread use of condoms and low prevalence of sexually transmitted diseases in Danish non-drug addict prostitutes. Brit. Med. J. 293:1473-1474.

111. Philpot CR, Harcourt C, Edwards J, Grealis A. (1988). Human immunodeficiency virus and female prostitutes, Sydney 1985. Genitourinary Med. 64:193-7.

112. Philpot CR, Harcourt CL, Edwards JM. (1991). A survey of female prostitutes at risk of HIV infection and other sexually transmissible diseases. Genitourinary Med. 67:384-8.

113. Pineda JA, Aguado I, Rivero A, et al. (1992). HIV-1 infection among non-intravenous drug user female prostitutes in Spain. No evidence of evolution to Pattern II. AIDS 6:1365-1369.

114. McKeagney N, Barnard M, Leyland A, Coote I, Follet E. (1992). Female streetworking prostitution and HIV infection in Glasgow. Brit. Med. J. 305:801-804.

115. Anonymous. (1993). HIV infection in European female sex workers: epidemiological link with use of petroleum-based lubricants. European Working Group on HIV Infection in Female Prostitutes. AIDS 7:401-8.

116. Anonymous. (1998). The HIV/AIDS/STD epidemics in Asia and the Pacific. Australian HIV Surveillance Report 14:1-8.

117. Samrith C. Official HIV and AIDS Case Report. Phnom Penh: World Health Organisation, 1997.

118. McLaws ML, Brown ARD, Cunningham PH, Imrie AA, Wilcken B, Cooper DA. (1989). Prevalence of maternal HIV infection based on anonymous testing of neonates, Sydney 1989. Med. J. Aust. 153:383-386.

119. Lundberg GD. (1988). Serological diagnosis of human immunodeficiency virus infection by Western Blot testing. JAMA 260:674-679.

120. Wooldridge HCM, Services MfHaF. Copy of letter sent to Senator Christopher Ellison, 1997.

121. Phair J, Jacobson L, Detals R, et al. (1992). Acquired Immune Deficiency Syndrome Occuring Within 5 Years of Infection with Human Immunodeficiency Virus Type-1: The Multicenter AIDS Cohort Study. J. Acquir. Immun. Defic. Syndr. 5:490-496.

122. Melbye M, Begtrup K, Rosenberg PS, et al. (1998). Differences in susceptibility to AIDS development: A cohort study of Danish and American homosexual-bisexual men, 1981-1995. J. Acq. Immune Def. Syndr. Hum. Retrovirol. 18:270-276.

123. Lemp GF, Porco TC, Hirozawa AM, et al. (1997). Projected incidence of AIDS in San Francisco: The peak and decline of the epidemic. J. Acq. Immune Def. Syndr. Hum. Retrovirol. 16:182-189.

124. St. Louis ME, Rauch KJ, Peterson LR, Anderson JE, Schable CA, Dondero TJ. (1990). Seroprevalence rates of human immunodeficiency virus infection at sentinel hospitals in the United States. NEJM 323:213-218.

125. Burke DS, Brundage JF, Redfield RR, et al. (1988). Measurement of the false positive rate in a screening program for human immunodeficiency virus infections. NEJM 319:961-964.

126. Dax E. (1994). The HIV Western blot: Reply to letter. Med. J. Aust. 160:808.

127. Kion TA, Hoffmann GW. (1991). Anti-HIV and anti-anti-MHC antibodies in alloimmune and autoimmune mice. Science 253:1138-1140.

128. Genesca J, Jett BW, Epstein JS, Shih JWK, Hewlett IK, Alter HJ. (1989). What do Western Blot indeterminate patterns for Human Immunodeficiency Virus mean in EIA-negative blood donors? Lancet ii:1023-1025.

129. Kozhemiakin LA, Bondarenko IG. (1992). Genomic instability and AIDS. Biochimiia 57:1417-1426.

130. Strandstrom HV, Higgins JR, Mossie K, Theilen GH. (1990). Studies with canine sera that contain antibodies which recognize human immunodeficiency virus structural proteins. Cancer Res. 50:5628s-5630s.

131. Kashala O, Marlink R, Ilunga M, et al. (1994). Infection with human immunodeficiency virus type 1 (HIV-1) and human T cell lymphotropic viruses among leprosy patients and contacts: correlation between HIV-1 cross-reactivity and antibodies to lipoarabinomannan. J. Infect. Dis. 169:296-304.

132. Mason AL, Xu L, Guo L, et al. (1998). Detection of retroviral antibodies in primary biliary cirrhosis and other idiopathic biliary disorders. Lancet 351:1620-1624.

133. Chant K, Lowe D, Rubin G, et al. (1993). Patient-to-patient transmission of HIV in private consulting surgical consulting rooms. Lancet 342:1548-1549.

134. Turner VF, Papadopulous-Eleopulos E. (1994). Patient to patient transmission of HIV in a surgeon's private rooms: Invited deposition to the Royal Australasian College of Surgeons. At website www.virusmyth.com/aids/perthgroup/ .

135. Sinoussi F, Mendiola L, Chermann JC. (1973). Purification and partial differentiation of the particles of murine sarcoma virus (M. MSV) according to their sedimentation rates in sucrose density gradients. Spectra 4:237-243.

136. Toplin I. (1973). Tumor Virus Purification using Zonal Rotors. Spectra 225-235.

137. Bess JW, Gorelick RJ, Bosche WJ, Henderson LE, Arthur LO. (1997). Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations. Virol. 230:134-144.

138. Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ. (1997). Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations. Virol. 230:125-133.

139. Beard JW. (1957). Physical methods for the analysis of cells. Ann. N. Y. Acad. Sci. 69:530-544.

140. Grafe A. (1991). A history of experimental virology. Heidelberg: Springer-Verlag, 1991.

141. Panem S. (1979). C Type Virus Expression in the Placenta. Curr. Top. Pathol. 66:175-189.

142. Gallo RC, Wong-Staal F, Reitz M, Gallagher RE, Miller N, Gillepsie DH. Some evidence for infectious type-C virus in humans. (1976). p. 385-405 In: Animal Virology Balimore D, Huang AS, Fox CF, eds Academic Press Inc., New York.

143. Hockley DJ, Wood RD, Jacobs JP. (1988). Electron Microscopy of Human Immunodeficiency Virus. J. Gen. Virol. 69:2455-2469.

144. Lecatsas G, Taylor MB. (1986). Pleomorphism in HTLV-III, the AIDS virus. S. Afr. Med. J. 69:793-794.

145. O'Hara CJ, Groopmen JE, Federman M. (1988). The Ultrastructural and Immunohistochemical Demonstration of Viral Particles in Lymph Nodes from Human Immunodeficiency Virus-Related Lymphadenopathy Syndromes. Hum. Pathol. 19:545-549.

146. Varmus H. (1987). Reverse Transcription. Sci. Am. 257:48-54.

147. Varmus HE. (1989). Reverse transcription in bacteria. Cell 56:721-724.

148. Gallo RC, Sarin PS, Wu AM. On the nature of the Nucleic Acids and RNA Dependent DNA Polymerase from RNA Tumor Viruses and Human Cells. (1973). p. 13-34 In: Possible Episomes in Eukaryotes Silvestri LG, ed North-Holland Publishing Company, Amsterdam.

149. Tomley FM, Armstrong SJ, Mahy BWJ, Owen LN. (1983). Reverse transcriptase activity and particles of retroviral density in cultured canine lymphosarcoma supernatants. Br. J. Cancer 47:277-284. 150. Christie H. Interview with Dr. Robert Gallo July 1st Palexpo Conference Centre Geneva. [Betacam]. New York, 1998.

151. Peuchmaur M, Delfraissy JF, Pons JC, et al. (1991). HIV proteins absent from placentas of 75 HIV-1-positive women studied by immunohistochemistry. AIDS 5:741-5.

152. Faulk WP, Labarrere CA. (1991). HIV proteins in normal human placentae. American Journal of Reproductive Immunology 25:99-104.

153. Stott EM. (1991). Anti-cell antibody in macaques. Nature 353:393.

154. Arthur LO, Bess JW, Jr., Urban RG, et al. (1995). Macaques immunized with HLA-DR are protected from challenge with simian immunodeficiency virus. J. Virol. 69:3117-24.

155. Eigen M, Schuster P. (1977). The hypercycle. Die Naturwissenschaften 64:541-565.

156. Eigen M, Gardiner W, Schuster P, Winkler-Oswatitsch R. (1981). The origin of genetic information. Sci. Am. 224:78-94.

157. Gallagher RE, Gallo RC. (1975). Type C RNA Tumor Virus Isolated from Cultured Human Acute Myelogenous Leukemia Cells. Science 187:350-353.

158. Barbacid M, Bolognesi D, Aaronson SA. (1980). Humans have antibodies capable of recognizing oncoviral glycoproteins: Demonstration that these antibodies are formed in response to cellular modification of glycoproteins rather than as consequence of exposure to virus. Proc. Natl. Acad. Sci. U S A 77:1617-1621.

159. Snyder HW, Fleissner E. (1980). Specificity of human antibodies to oncovirus glycoproteins: Recognition of antigen by natural antibodies directed against carbohydrate structures. Proc. Natl. Acad. Sci. U S A 77:1622-1626.

160. Kurth R, Teich NM, Weiss R, Oliver RTD. (1977). Natural human antibodies reactive with primate type-C antigens. Proc. Natl. Acad. Sci. U S A 74:1237-1241.

161. Casarett DJ, Lantos JD. (1998). Have we treated AIDS too well? Rationing and the future of AIDS exceptionalism. Ann. Int. Med. 128:756-759.

162. Anonymous. (1998). The National AIDS Registry. Australian HIV Surveillance Report 14:14.

163. Balter M. (1998). Europe: AIDS research on a budget. Science 280:1856-1858.

164. Stine GJ. Testing for Human Immunodeficiency Virus. (1995). p. 231 In: AIDS Update 1994-1995 Prentice Hall, New Jersey.

165. Glover E. (1998). French panel calls for closer monitoring of genetic modification. Nature 394:4.