Make your own free website on

The Yin & Yang of HIV

Part 1 of 3

Supporters of the 'HIV causes AIDS' hypothesis cannot back up their claims with scientific evidence, yet they continue to reject alternative explanations and promote life-threatening drug treatments.

(Go to Part 1, 2, 3)

Extracted from Nexus Magazine, Volume 6, Number 4 (June-July 1999).
PO Box 30, Mapleton Qld 4560 Australia.
Telephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381
From our web page at:

© 1999 by Valendar F. Turner
Department of Emergency Medicine
Royal Perth Hospital
Perth, Western Australia
telephone +61 (0)8 9224 2662
fax +61 (0)8 9224 7045

and Andrew McIntyre
Freelance Journalist
Melbourne, Victoria, Australia

A theory is a good theory if it satisfies two requirements: It must accurately describe a large class of observations on the basis of a model that contains only a few arbitrary elements, and it must make definite predictions about the results of future observations.
- Dr Stephen Hawking


The notion that HIV/AIDS is infectious and sexually transmitted is based on a relationship between antibodies claimed specifically induced by a retrovirus, HIV, and particular diseases in certain risk groups. However, the HIV theory has been challenged for well over a decade in many scientific publications, principally by Peter Duesberg from the USA and Eleni Papadopulos-Eleopulos and her colleagues in Perth, Western Australia.

Failure of HIV/AIDS to spread beyond the original risk groups and particularly to Western heterosexuals, especially non-drug-using prostitutes, signals that the HIV theory of AIDS is in need of urgent reappraisal. This has serious implications for both the way science has been conducted and for public health policy and planning. The HIV theory has cost billions of dollars and locked in enormous amount of energy in research by thousands of scientists worldwide. So far, it has yet to save a single life.

There is an urgent need to establish a truly independent and distinguished international committee to review the current theories and those that challenge them. There needs to be a co-operative but urgent reassessment of AIDS.



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 few years leading up to the AIDS era and the discovery of HIV are illuminating. It was a time when a promiscuous minority of young, "liberated" gay men in a few large American cities were increasingly developing previously uncommon diseases such as fatal forms of the malignancy Kaposi's sarcoma and a fungal pneumonia known as PCP.

At the time, whilst it was reasonable to implicate an infectious microbe transmitted by rampant, indiscriminant sexual practices interspersed with needle sharing and drug taking, the fact that immune suppression had multiple causes was also known in 1981. Some considered the diseases resulted from multiple assaults to bodily functions caused by the many and varied diseases, toxins and treatments that accompanied the gay and drug-taking lifestyle that had evolved during the late 1970s.

Just how extensive these multiple assaults were was indicated by the English journalist Neville Hodgkinson, documenting the range of infections of just one homosexual, the late Michael Callen, in his book, AIDS - The failure of contemporary science: How a virus that never was deceived the world.29 Hodgkinson writes: "From 1973, when he came out as a homosexual, to 1975, he only got mononucleosis and non-specific urethritis (NSU). In 1975, he had his first bout of gonorrhoea... But from there, it all began to snowball. 'First came hepatitis A in 1976 [said Callen]. Then more NSU and gonorrhoea. In 1977, amoebas [intestinal parasites] and hepatitis B...NSU and gonorrhoea. 1978: more first case of shigella [and] more VD. Then in 1979, hepatitis a third time...non-A, non-B...amoebas...giardias...a fissure [and] my first case of syphilis. And of course, more gonorrhoea [penile, anal and oral]. In 1980: the usual gonorrhoea, shigella twice, and more amoebas...' Added to that list were herpes simplex types I and II; venereal warts; salmonella; chlamydia; cytomegalovirus (CMV); Epstein-Barr virus (EBV); mononucleosis; and finally cryptosporidiosis ('a disease of cattle!')." Indeed, an early US Centers for Disease Control (CDC) study confirmed that the first 100 men with AIDS had a median lifetime number of 1,120 sexual partners.30 As Callen himself put it: "By 1981, I got some combination of venereal diseases each and every time I had sex."

Not surprisingly, given the widespread belief of a causal relationship between immunity and the maintenance of health, in 1981 the "new" disease became known as Gay Related Immune Deficiency (GRID). In fact, none of the diseases was new. Some were known to occur in drug addicts and haemophiliacs long before the AIDS era.64, 65 What was "new" was their exponentially escalating prevalence in gay men.



Coincidental with the beginning of the AIDS era, a technique was developed to classify and count the different types of lymphocyte white blood cells. It was noticed that some AIDS patients had diminished numbers of the so-called T4 "helper" cell subtype and, despite lack of proof, the cells were assumed to be dying at the behest of an agent selectively targeting them. This became the "hallmark" of AIDS as well, forming a measure of the amount of immune deficiency. In turn, this "immune deficiency" (the "AID" in AIDS) caused the diseases (the "S" in AIDS) that constitute the clinical syndrome. The perceptions that T4 cells were dying and AIDS was infectious led to the theory that AIDS is caused by a microbial organism.

Five years prior to the AIDS era, a few laboratories around the world were drawing towards the end of a fruitless search to prove a viral cause for human cancers. During the 1970s, Dr Robert Gallo, the central figure as "co-discoverer" of the AIDS virus, and his colleagues claimed to have discovered three human retroviruses. (The name "retroviruses" arises because of the copying of the RNA which forms the viral "genes" [the genome] "backwards" into DNA - a direction contrary to that long considered universal, that is, from DNA into RNA.)

In 1975, the first human retrovirus, HL23V, was proposed to cause human leukaemia, but by 1980 was considered an embarrassing mistake - in fact, not to have ever existed. Of the remaining two, one was postulated to cause a specific, though rare, form of adult leukaemia, and the second remains orphaned without a disease. What is significant is that the latter two retroviruses are said to exhibit a liking for T4 lymphocytes.

This led Donald Francis, Gallo and others to propose that an existing or closely related retrovirus was the agent responsible for killing the T4 cells in AIDS patients. When researchers actively sought and then discovered the same diseases in individuals who were not gay, retroviruses, as well as retrovirologists, received renewed interest and GRID became AIDS.



In May 1983, Professor Luc Montagnier and his colleagues at the Pasteur Institute in Paris published a paper in Science, entitled "Isolation of a T-Lymphotrophic Retrovirus from a Patient at Risk for Acquired Immune Deficiency Syndrome (AIDS)".66 It is important to note that the first word in this paper, "Isolation", serves as a signal that the researchers are claiming proof for the existence of a new virus.

In the interests of science, on several occasions Montagnier sent samples of his tissue cultures to the Gallo laboratory in America, with the express understanding that these "could be used for biomedical, biological and molecular biological studies".67 However, Montagnier did not claim to have proven his virus was the cause of AIDS, and the French discovery lay on the table until May 1984 when Gallo and Popovic and their colleagues published four papers, also in Science.68-71

On 23 April 1984, at a Washington press conference held two weeks before the papers were published, Margaret Heckler, Secretary for Health and Human Services (HSS), announced that Gallo and his co-workers had discovered the "probable" cause of AIDS and had developed a sensitive blood test to detect the virus in the body. A curative vaccine was predicted within two years. Inexplicably, causation was proclaimed merely by association and despite "isolation" of HIV in only 26 (i.e., 36 per cent) of Gallo's 72 AIDS patients - barely a third. (The frequency of "isolation" is no better today.72)

In 1985, the Pasteur Institute alleged that Gallo had misappropriated their virus. The ensuing conflict, which eventually reached the US courts, was settled by a negotiated agreement signed in 1987 by Gallo and Montagnier as "co-discoverers", and US President Reagan and French Premier Chirac. Nevertheless, the matter drew the attention of John Crewdson, an investigative journalist, and US Senator John Dingell. In November 1989, Crewdson published a lengthy article in the Chicago Tribune newspaper, which provoked an internal NIH enquiry into suspect data from Gallo's laboratory.

A draft report of the formal investigation, written by the NIH Office of Scientific Integrity (OSI), was published in September 1991, in which the principal author, Mikulas Popovic, was accused "of misconduct for misstatements and inaccuracies" that appeared in the first Science paper, and suggesting that Gallo, as laboratory chief, "created and fostered conditions that give rise to falsified/fabricated data and falsified reports".

The OSI's final draft report, completed in January 1992, was immediately criticised, and was followed by a review of the OSI report by the Office of Research Integrity (ORI) which found Gallo guilty of scientific misconduct.

Nonetheless, even after this long investigation and its conclusion, the US Government withdrew its findings following Gallo's announcement of an appeal. Despite this, in 1994, US officials credited Montagnier and his colleagues as the discoverers of HIV and yielded the French a greater share of royalties from the HIV antibody tests. In taking these unprecedented steps, Dr Harold Varmus, the Director of the NIH, acknowledged that "scientists at the NIH used a virus provided to them by Institut Pasteur to invent the American test kit". This action scarcely vindicated the Dingell report which had concluded that the settlement "barely managed to paper-over the glaring, unresolved issues". Rather, it was the culmination of a cover-up where "political and international reputational imperatives" at HHS "assumed pre-eminence over scientific integrity", while defending Gallo's claim became "tantamount to defending the US Government itself".73

According to Eleopulos and her colleagues, regardless of the material uncovered by the OSI, Gallo's data, which still remains the best of its kind, does not prove the existence of HIV and, even if it did, nowhere in the papers is there proof that HIV causes AIDS.16, 21



In December 1987, three and a half years after the Washington press conference, Professor Peter Duesberg, virologist and molecular biologist at the University of California, Berkeley, published an invited paper entitled "Retroviruses as Pathogens: Expectations and Reality".3 Duesberg was a much fêted scientist, considered to be "the golden boy of virology" and "the greatest living retrovirologist". He had developed many of the laboratory techniques for studying retroviruses and their genetic make-up, had discovered cancer-causing genes, and was recipient of a $350,000 "outstanding investigator" award from the NIH.

But Duesberg dropped a bombshell. He asserted that, apart from the relatively few cancer-causing retroviruses, the majority are virtually harmless. Duesberg argued that HIV is neutralised by antibodies shortly after infection and thus antibodies signal its containment. He also pointed to data proving that well, sick or dying-from-AIDS, HIV-positive individuals contain insufficient amounts of HIV to do harm. Even if HIV were to kill all the T4 cells it had infected every 1 to 2 days, the number of T4 cells needing replacement approximated the amount of blood shed by a man cutting himself shaving.

For the protagonists, the low "viral burden" - that is, the amount of "HIV DNA" in cells - was a fact that no one, not even Gallo, could satisfactorily reconcile with an immunity-destroying pathogen killing gay men within a year or two of diagnosis. However, rather than addressing this as a scientific problem warranting dialogue with someone known to have considerable knowledge of the subject, Duesberg's questions antagonised Gallo to the point where he refused to discuss the matter. Meetings convened to deal with the uncomfortable implications of Duesberg's paper were suddenly cancelled at the highest level.

In 1989, Duesberg presented further argument.4 HIV does not fulfil the postulates that 19th century bacteriologist Robert Koch had developed to prove a microbe causes a disease. These four postulates are: (a) the organism must be present in all cases of the disease; (b) it must be grown and then isolated in pure culture from the cells of individuals with the disease; (c) it must reproduce the disease when introduced into a susceptible host or experimental animals, (d) from where it must once again be recovered.

According to Duesberg: "From every angle, HIV fails Koch's first postulate." The second postulate was fulfilled but only by subjecting cells to drastic chemical manipulation that did not approach conditions in vivo. (Eleopulos has argued how basic retrovirology has long shown that oxidation which prevails in HIV/AIDS patients and their cell cultures creates internal [endogenous] retroviruses in cells whose DNA was not previously infected from the outside.12, 14, 15, 74, 75 One per- cent of human DNA, that is, an amount 3,000 times larger than "HIV" DNA, is made up of endogenous retroviral DNA.76)

The third postulate failed because, as Duesberg points out: "During the past decade, more than four hundred thousand AIDS patients have been treated and investigated by a system of five million medical workers and AIDS researchers, none of whom [has] been vaccinated against HIV... But ten years later there is not even one case in the scientific literature of a health worker who ever contracted presumably infectious AIDS from a patient... AIDS is not infectious." Similarly, "nine years after the NIH first started infecting chimpanzees with HIV - over 150 so far at a cost of $40,000-50,000 apiece", all "are still healthy".5**

In 1992, Duesberg shifted focus from HIV to argue that "AIDS [is] acquired by drug consumption and other noncontagious risk factors".5 Apart from illicit and recreational drugs, Duesberg's list included the first "anti-retroviral" drug, zidovudine (AZT). In other words, a specific treatment for HIV infection was postulated to be a cause of AIDS.

Duesberg continued to regard HIV as bona fide, but as an inert, harmless "passenger" virus linked to AIDS only through the kinds of activity associated with drug taking (including taking of prescribed drugs). Duesberg, like others before him, pointed to the epidemiological data revealing a 50-fold difference in the AIDS "attack rate" between various groups of HIV-positive individuals, as well as the proclivity of certain AIDS diseases for particular risk groups. Thus, 50 per cent of HIV-positive blood transfusion recipients develop AIDS within one year (but so do 50 per cent of HIV negatives) compared to 1 per cent of haemophiliacs. Kaposi's sarcoma was, for all intents and purposes, confined to gay men.5,13,77 Thus, even if HIV were necessary to cause AIDS, it could not be the only factor. However, accretion of "co-factors" to the HIV theory rendered the significance of any particular factor problematic. It was possible to argue that HIV may be only a minor factor or, at least in the minds of Eleopulos and Duesberg, not a factor.

Apparently, the role of HIV was also a problem for Montagnier. Although he wrote in Nature in December 1984 that "all available data are consistent with the virus being the causative agent of AIDS",78 in 1985 he expressed an opinion impossible to reconcile with the HIV theory. "This syndrome occurs in a minority of infected persons, who generally have in common a past of antigenic stimulation and of immune depression before LAV [HIV] infection",79 that is, cause after effect (italics ours). One must surmise that, within a year, the discoverer of HIV was already hedging his bets. His recent interview with the investigative journalist Djamel Tahi61 (see below) fuels such speculation.



Eleni Papadopulos-Eleopulos' AIDS research began in 1981. In May 1986, she submitted for publication a paper which refuted every step in the HIV theory, including HIV itself. She also proposed an alternative, non-viral theory (of which "Duesberg's" "Drugs/ AIDS hypothesis" is a subset), and predicated non-toxic and relatively inexpensive treatments.

Her theory was based on a general theory of cellular functioning, which she had formulated in the 1970s as a basis for unravelling the genesis and improving the treatment of cancer and to offer fresh insights into the pathogenesis of cardiovascular diseases and ageing. Eleopulos postulates that normal cellular functioning is determined by the level and oscillations of cellular redox23 (oxidation and its chemical opposite, reduction). In her view, when oxidation is prolonged or excessive, cells become abnormal, injured and susceptible to diseases.

Eleopulos had noticed a link between the risk groups. Gay men, drug users and haemophiliacs are exposed to chemical stressors in the form of semen, nitrites, illicit drugs and factor VIII (the blood-clotting protein missing from and administered to haemophiliacs). There is abundant evidence that these substances are potent cellular oxidants.12 In Eleopulos' view, oxidative stress produces low numbers of T4 cells and AIDS, as well as the phenomena inferred as proof for the existence of HIV.

The ready acceptance of the Montagnier/Gallo 1983/84 Science papers posed enormous difficulties for Eleopulos in having her work published. Thus, "Reappraisal of AIDS: Is the oxidation caused by the risk factors the primary cause?" was twice rejected by Nature, eventually finding light of day in Medical Hypotheses, twelve months after Duesberg.12 However, the editor of this journal had also rejected the paper, only recanting after Eleopulos worked for several months to convince him that equatorial Africa was not in the grip of an epidemic of sexually transmitted immunodeficiency and thus not in breach of her theory.11, 24, 63, 80

To paraphrase the theoretical physicist Stephen Hawking: wrong predictions affirm bad theories; correct predictions make them powerful. The HIV theory requires that HIV causes all the AIDS-defining diseases and predicts that HIV/AIDS will become a global epidemic via the oldest and most unstoppable of all human activities. However, Kaposi's sarcoma, one of the two diseases for which the HIV theory was proposed, is no longer attributed either directly or indirectly (via AID) to HIV.12, 13, 54, 77, 81***

In the OECD countries, the prediction of a sexual pandemic has failed completely. For example, as of the beginning of 1998, 93 per cent of the cumulative deaths from AIDS in Australia occurred in the original risk groups, that is, gay/bisexual men, drug addicts and haemophiliacs. This observation fits the classic demographic profile of non-infectious diseases such as pellagra, beri-beri and scurvy which characteristically remain confined to their risk groups. All are caused by vitamin deficiencies, but in the past were regarded as infectious and sufferers were shunned and quarantined.

The HIV protagonists also predicted a curative vaccine by the end of 1986 and an animal model to prove the HIV theory beyond all doubt. Neither prediction has been fulfilled. A vaccine is not envisaged until well into the next century, possibly around 2010, and animals given "HIV" do not develop AIDS.

On the other hand, the Eleopulos oxidative stress theory predicts the current demographic data, an apparent loss of T4 cells, the risk from passive anal intercourse in both sexes, HIV positive and AIDS patients being oxidised relative to normal individuals, the amelioration of HIV/AIDS by the use of antioxidants, and a non-infectious animal model. Every one of these predictions has materialised. Oxidative stress is well established by hundreds of papers,14, 62, 82-84 so much so that in the early 1990s the Pasteur Institute was advertising international scholarships for study into the phenomenon. In fact, last year Luc Montagnier became the principal editor of a 558-page book devoted to oxidative stress in cancer, ageing and AIDS.85

The Eleopulos theory predicts that a decline in T4 cells can occur without cellular death. In fact, according to the Perth group, there is no evidence to support the notion that T4 cells are dead or that "HIV" kills such cells. In T4 cell cultures, the same number of T4 cells "disappear", regardless of whether one adds "HIV" or merely the chemical stimulants obligatory to "grow" the "HIV".86 Neither is there proof that low numbers of T4 cells are either necessary or sufficient to produce the clinical syndrome.9,12,14 This is a view recently expressed by leading HIV/AIDS scientists such as Dr Arthur Anderson from the US Army Medical Research Institute of Infectious Disease87 and Dr Zvi Grossman at the University of Tel Aviv.88

In other words, the central tenet of the HIV theory - virus-induced killing of immune cells leading to AIDS - is now being questioned by HIV/AIDS experts themselves. Nonetheless, and despite so much evidence to the contrary, the orthodox view remains entrenched. In fact, since 1993, the low number of T4 cells has been enshrined in the 1993 CDC AIDS definition whereby AIDS can be diagnosed without a disease. Just as "co-factors" were proposed to rescue the HIV theory in the mid 1980s, in July 1998 Chen and colleagues from the UCLA AIDS Institute, School of Medicine, Los Angeles, reported evidence that "naturally non-infectious virus" or virus "rendered defective" by "anti-HIV" drugs could still contribute to the loss of T4 cells throughout the course of HIV disease.89 In other words, "alive" or "dead", HIV causes immune deficiency. Such a proposal does not augur well for the use or continued development of "anti-HIV" drugs.

Consistent also with the Eleopulos oxidative stress theory is the direct relationship between high frequencies of passive anal intercourse and the development of AIDS, as well as the fact that the only animal model of AIDS is non-infectious. Mice repeatedly injected with foreign cellular proteins develop a dramatic depletion of T4 cells and Kaposi's sarcoma-like tumours, and "abundant" retrovirus-like particles appear in their spleens.90 Thus AIDS diseases are followed by the production of retrovirus-like particles, and not the other way around.

To the uninitiated this may seem perplexing, but it is well recognised that retroviral particles appear de novo in cell cultures not previously infected, because all cells contain retroviral information carried in the germ line DNA.76 Indeed, according to distinguished retrovirologists such as Weiss and Temin, new retroviral DNA arises by rearrangement of cellular DNA, caused by many factors including pathological processes - a view that concedes retroviruses an effect and not the cause of diseases.74, 75



It would take a second article to discuss AZT and the many other "anti-HIV" drugs. Suffice it to say there is no scientific proof that such drugs kill "HIV" or cure AIDS, but there is ample evidence they are harmful.1, 53, 56, 91

In 1994, a double-blind randomised comparison of two policies of AZT treatment (immediate and deferred) was reported (the Concorde trial). This involved 1,749 symptom-free, HIV-infected individuals from centres in the UK, Ireland and France. The 347 clinical endpoints (AIDS and death) outnumbered the total of those in all other published trials in symptom-free and early symptomatic infection. The results showed "there was no statistically significant difference in clinical outcome between the two therapeutic policies".92 In 1995, extended results of Concorde showed a significant increased risk of death among the patients treated early.

However, despite these data, despite disclaimers that patients treated with AZT may continue to develop the AIDS diseases, that the side effects of AZT may mimic AIDS, and that AZT given to non-HIV-infected babies causes the AIDS-defining pneumonia, PCP,93 AZT continues to be the most commonly prescribed anti-HIV drug.

Dr Donald Abrams, Professor of Medicine and Director of the AIDS program at San Francisco General Hospital, said: "I have a large population of people who have chosen not to take any anti-retrovirals... I've been following them since the very beginning... They've watched all of their friends go on the antiviral bandwagon and die."94

Indeed, even an elementary study of the pharmacological literature reveals that AZT cannot be an anti-HIV drug; it is toxic to all cells.91 In fact, what unites long-term survivors of AIDS is their resolve not to take "anti-retrovirals".95-97

In mid-1996, the latest drugs, the "protease inhibitors" (PIs), were introduced. These are prescribed as one of up to 250 possible combinations of "cocktails" with AZT or similar drugs as "highly active anti-retroviral therapy" (HAART). Detailed data on these drugs, of the kind usually reserved for medical practitioners, appear regularly in glossy, multi-page advertisements in gay men's magazines.

At the July 1996 11th International AIDS Conference, Time magazine Man of the Year David Ho predicted that scientists would "find new drugs to wipe HIV out of the body within three years, possibly within just one".98 At the July 1998 XIIth AIDS conference, Ho stated it will take at least 10 years of intense combination drug therapy to kill off all the HIV in an infected person's body, but that a sizeable percentage of HIV patients will never get close. Many patients cannot tolerate the untoward effects of these "cocktails", and measurements show that the DNA "viral" burden does not decrease significantly.99-102 According to Kaufmann et al.: "49% of people taking HAART, who were followed by the Swiss HIV Cohort Study, did not have viral suppression, and similar data are emerging from other centres."103

In the May 1998 Proceedings of the National Academy of Sciences, Dr William Paul, former Director of the National Institutes of Health's Office of AIDS Research, wrote: " matter how long a person is treated with anti-HIV drugs, there will always be new will have to be treated forever... No one is getting cured... This bodes extremely poorly for combination therapy as something curative..."88

Dr Michael Saag, at the University of Alabama, Birmingham, USA, is responsible for the treatment of over 1,000 AIDS patients. His treatment is state-of-the-art and his clinic is sought- after by pharmaceutical companies to conduct trials on their newest compounds. In a recent interview, Dr Saag said: "Perhaps the biggest difference between the cure paradigm and whatever paradigm we're in now is, we now should expect failure with whatever [HAART cocktails] we first use. We should plan on it. We should prepare for it. Clinicians should expect failure." Saag warns the HAART "'dam' is already leaking and there's high danger of it collapsing altogether. Failures are occuring right and left." Speaking about his dying patients: "They aren't dying of traditionally defined AIDS illness... I don't know what they're dying of, but they are dying. They're just wasting and dying... It is sobering...while we are making good guesses, they are just guesses. We don't know what we are doing."104

Given the toxicity of these drugs, it is unlikely anyone can tolerate taking them for more than a few years. If this outlook is gloomy for HIV/AIDS sufferers, it is even worse considering there is no substantial, alternative therapeutic strategy anywhere on the horizon.

The futility of all "anti-HIV" drugs, past, present and future, is best highlighted in a June 1998 interview by Dr Harold Varmus, Nobel Laureate retrovirologist and Director of the National Institutes of Health: "Trying to rid the body of a virus whose genome is incorporated into the host genome may be impossible."105



The longevity of the HIV theory has been considerably boosted by the virtual refusal of editors of leading medical journals to publish any material which takes HIV to task. Without these data, and the stamp of approval engendered by such publication, it is almost impossible for the debate to reach the ears of those who matter the most: clinicians and their patients. Like generals directing wars, the remoteness of editors begets an objectivity which, while essential to clear thinking, militates against an appreciation of the profound responsibilities editors hold at the bedside.

Ultimately, although the HIV theory is manifoldly problematic, physicians, patients, relatives, politicians, journalists and the tax-paying public are systematically denied knowledge of its existence and substance. Not only is there is a total absence anywhere of a disinterested, adjudicated debate, but individuals, whose only motivation is to contribute to solving a disease claimed to afflict millions of people, find themselves censored. For example, Sir John Maddox, former editor of the world's most prestigious science journal, Nature, denied Duesberg the right of reply on issues he raised because his views give "many infected people the belief that HIV infection is not in itself the calamity it is likely to prove".29 Yet, in a recent edition of the same journal, but in another context, there is a claim that "the voice of sceptics may grow tiresome, but the mainstream is in trouble if it cannot win a public debate with them".

Officials at the Berlin 10th International AIDS Conference confiscated Dutch AIDS analyst Robert Laarhoven's press pass and threatened him with expulsion from Germany for "criminal trespass" because he placed copies of the dissident journal Rethinking AIDS on an "unauthorised" table.

Nature has repeatedly rejected every paper and letter submitted by Eleopulos and her colleagues since 1986, without providing a single scientific reason and invariably citing space constraints in the journal. Not even the profound implications of the Tahi/Montagnier interview are of any apparent concern to Nature. Professor John Kaldor, one of Australia's foremost "established experts" on AIDS, admits that dissidents "intersperse their cases with grains of fact".106 However, because of Kaldor and colleagues' "strong instinct not to dignify the sceptics' arguments by attempting to refute them", arguments based on these "grains of fact" and many other data remain unanswered and unresolved.


Editor's note:
The second part of this article will examine the many scientific problems with the HIV theory of AIDS.

Continued next issue of NEXUS...

* US journalist Christine Johnson's interview (now available in six languages) with the leader of the Perth group was reviewed by scholar and international gay media personality Professor Camille Paglia in her column in the US Salon magazine (28 October 1997): "For a superb critique of the scandalously overpoliticized scientific research on AIDS, see Christine Johnson's long interview with Australian biophysicist Eleni Papadopulos-Eleopulos in the new issue of the British AIDS magazine, Continuum [vol. 5, no. 1, autumn 1997]. The American major media have effectively suppressed longstanding questions about whether the AIDS test is reliable or whether an HIV virus in fact exists at all."

** On 5 May 1998, two US Republicans said they were exploring ways to give a comfortable retirement to 1,500 chimpanzees that were bred for AIDS research. Accompanied by primate expert Jane Goodall, House Speaker Newt Gingrich and Rep. Jim Greenwood (R-Penn.) said they were working on a bill to set up sanctuaries for the chimps. The chimps, bred in the United States specifically for AIDS research, did not turn out to be the effective models that scientists had anticipated. With no research use, the primates that are man's closest cousins are languishing in cages at an annual cost of US$7.3 million.

*** In 1988, Eleopulos' paper that HIV does not cause Kaposi's sarcoma was thrice rejected by the Medical Journal of Australia on the advice of an "established expert". The reviewer stated: "The author tries to argue that Kaposi's sarcoma cannot be caused by HIV infection, and that therefore AIDS is not due to HIV infection. The arguments put forward by the author are quite unsatisfactory, and are not supported by even a desultory reading of the literature quoted. In addition, the author fails to examine the body of epidemiological, immunological and cellular literature concerning the pathology, pathogenesis and clinical associations of this fascinating manifestation of HIV infection." Yet this is the very "epidemiological, immunological and cellular literature" which eventually led the "established experts" to accept that "this fascinating manifestation of HIV infection" is not caused by HIV infection.


1. Duesberg, P.H., Inventing the AIDS Virus, Regnery Publishing, Inc., Washington, USA, 1996.
2. Mullis, K.B., Dancing Naked in the Mind Field, Pantheon, 1998.
3. Duesberg, P.H. (1987), "Retroviruses as carcinogens and pathogens: Expectations and reality", Cancer Res. 47:1199-1220.
4. Duesberg, P.H. (1989), Human immunodeficiency virus and acquired immunodeficiency syndrome: correlation but not causation", Proc. Natl Acad. Sci. 86:755-764, USA.
5. Duesberg, P.H. (1992), "AIDS acquired by drug consumption and other noncontagious risk factors", Pharmacol. Ther. 55:201-277.
6. Duesberg, P.H. (1995), "Foreign-protein-mediated immunodeficiency in hemophiliacs with and without HIV infection", Genetica 95:51-70.
7. Duesberg, P. and Rasnick, D. (1997), "The drugs-AIDS hypothesis", Continuum 4:1s-24s.
8. Duesberg, P.H. (1996), "Peter Duesberg responds", Continuum 4:8-9.
9. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M., Hedland-Thomas, B., Causer, D., Page, B. (1995), "A critical analysis of the HIV-T4-cell-AIDS hypothesis", Genetica 95:5-24.
10. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M., Causer, D. (1995), "Factor VIII, HIV and AIDS in haemophiliacs: an analysis of their relationship", Genetica 95:25-50.
11. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M., 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, V.F., Papadimitriou, J.M. (1992), "Kaposi's sarcoma and HIV", Med. Hypotheses 39:22-9.
14. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M. (1992), "Oxidative stress, HIV and AIDS", Res. Immunol. 143:145-8.
15. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M. (1993), "Is a positive Western blot proof of HIV infection?", Bio/Technology 11:696-707.
16. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M. (1993), "Has Gallo proven the role of HIV in AIDS?", Emerg. Med. [Australia] 5:113-123.
17. Papadopulos-Eleopulos, E., Turner, V.F., Causer, D.S., Papadimitriou, J.M. (1996), "HIV transmission by donor semen", Lancet 347:190-1.
18. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M. (1996), "Virus Challenge", Continuum 4:24-27.
19. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M., Causer, D. (1996), "The Isolation of HIV: Has it really been achieved?", Continuum 4:1s-24s.
20. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M., Causer, D. (1997), "HIV antibodies: Further questions and a plea for clarification", Curr. Med. Res. Opinion 13:627-634.
21. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M., Causer, D. (1997), "A critical analysis of the evidence for the isolation of HIV"; at website <>.
22. Papadopulos-Eleopulos E., Turner, V.F., Papadimitriou, J.M., Causer, D. (1995), "A reply to Wei and Ho"; at website <>.
23. Papadopulos-Eleopulos, E. (1982), "A Mitotic Theory", J. Theor. Biol. 96:741-758.
24. Papadopulos-Eleopulos, E., Turner, V.F. (1994), "Deconstructing AIDS in Africa", The Independent Monthly 50-51.
25. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M., 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-Eleopulos, E., Turner, V.F., Papadimitriou, J.M., Causer, D. (1997), "Why no whole virus?", Continuum 4:27-30.
27. de Harven, E. (1997), "Pioneer deplores 'HIV'", Continuum 5:24.
28. Turner, V.F. (1994), "The HIV Western blot", Med. J. Aust. 160:807-808.
29. Hodgkinson, N., AIDS: The Failure of Contemporary Science, Fourth Estate, London, 1996.
30. Callen, M., Surviving AIDS, HarperCollins Publishers, 1991.
31. Johnson C. (1997), "Is HIV the cause of AIDS?" Continuum 5:8-19.
32. De Marchi, L. and Franchi, F., AIDS: la grande truffa, Edizioni SEAM, Rome, 1996.
33. Shenton, J., Positively False, I.B. Tauris, London, 1998.
34. Maggiore C., What if everything you thought you knew about AIDS was wrong?, HEAL, Los Angeles, 1997.
35. McDonald, J.F. (ed.), Genetica, Kluwer Academic Publishers, London, 1995.
36. Anonymous (1995), "Missing Virus: The Jody Wells Memorial Prize", Continuum 3:4.
37. Brody, S., Sex at Risk: Lifetime Number of Partners, Frequency of Intercourse, and the Low AIDS Risk of Vaginal Intercourse, Transaction Publishers, New Brunswick, NJ, 1997.
38. Caton, H., The AIDS Mirage, The University of New South Wales Press Ltd, Sydney, 1994.
39. Chirimuuta, R.C., Chirimuuta, R.J., Aids, Africa and Racism, R. Chirimuuta, Bretby House, Stanhope Bretby, Burton-on-Trent, UK, 1987, 1st ed.
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?", Provencetown 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", The Sunday Times, London, 22 May 1994, p. 24.
49. Hodgkinson, N., "World AIDS Conference", The European, 22-28 June 1998, pp. 30-31.
50. Konotey-Ahulu (1987), "AIDS in Africa: Misinformation and Disinformation", Lancet ii:206-207.
51. Koliadin, V.L. (1995), "Critical analysis of the current views on the nature of AIDS", Genetica 95:71-90.
52. Koliadin, V.L., "Some facts behind the expansion of the definition of AIDS in 1993", personal communication, 1997.
53. Lauritsen, J., The AIDS War, Asklepois Press, New York City, 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 < jlpoppers.htm>.
56. Lauritsen, J., Poison by Prescription: The AZT Story, Asklepois Press, New York, 1990.
57. Padian, N. and Pickering, J., "Female-to-male transmission of AIDS: a re-examination of the African sex ratio of cases", JAMA 256:590.
58. Root-Bernstein, R.S., Rethinking AIDS: The Tragic Cost of Premature Consensus, Macmillan, New York, 1993.
59. Root-Bernstein, R.S. (1995), "Five myths about AIDS that have miscredited research and treatment", Genetica 95:111-132.
60. Mullis, K.B. (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, 18 July 1997, Continuum 5:30-34.
62. Turner, V.F. (1990), "Reducing agents and AIDS: Why are we waiting?", Med. J. Aust. 153:502.
63. Turner, V.F. (1998), "Where we have gone wrong?", Continuum 5:38-44.
64. Rizza, C.R., Spooner, R.J.D. (1983), "Treatment of haemophilia and related disorders in Britain and Northern Ireland during 1976-80: Report on behalf of the directors of haemophilia centres in the United Kingdom", Br. Med. J. 286:929-933.
65. Johnson, R.E, Lawrence, D.N., Evatt, B.L., et al. (1985), "Acquired immunodeficiency syndrome among patients attending hemophilia treatment centers and mortality experience of hemophiliacs in the United States", Am. J. Epidemiol. 121:797-810.
66. Barré-Sinoussi, F., Chermann, J.C., 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.
67. Gallo, R.C., Sarin, P.S., Kramarsky, B., Salahuddin, Z., Markham, P., Popovic, M. (1986), "First isolation of HTLV-III", Nature 321:119.
68. Gallo, R.C., Sarin, P.S., Gelmann, E.P. (1983), "Isolation of Human T-Cell Leukemia Virus in Acquired Immune Deficiency Syndrome (AIDS)", Science 220:865-867.
69. Popovic, M., Sarngadharan, M.G., Read, E., Gallo, R.C. (1984), "Detection, Isolation, and Continuous Production of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and Pre-AIDS", Science 224:497-500.
70. 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.
71. Schupbach, J., Popovic, M., Gilden, R.V., Gonda, M.A., Sarngadharan, M.G., Gallo, R.C. (1984), "Serological analysis of a Subgroup of Human T-Lymphotrophic Retroviruses (HTLV-III) Associated with AIDS", Science 224:503-505.
72. World Health Organization (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.
73. Butler, D. (1995), "US accused of 'cover up' in defence of Gallo claims", Nature 373:372.
74. Temin, H.M. (1974), "On the origin of RNA tumor viruses", Harvey Lectures 69:173-197.
75. Weiss, R.A., Friis, R.R., Katz, E., Vogt, P.K. (1971), "Induction of avian tumor viruses in normal cells by physical and chemical carcinogens", Virol. 46:920-938.
76. 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. USA 93:5177-5184.
77. Beral, V.D., Bull, R., Darby, S. (1990), "Kaposi's sarcoma and sexual practices associated with faecal contact in homosexual or bisexual men with AIDS", Lancet 339:632-636.
78. Alizon, M., Sonigo, P., Barré-Sinoussi, P. et al. (1984), "Molecular cloning of lymphadenopathy-associated virus", Nature 312:757-760.
79. Montagnier, L. (1985), "Lymphadenopathy-Associated Virus: From Molecular Biology to Pathogenicity", Ann. Int. Med. 103:689-693.
80. Papadopulos-Eleopulos, E., Turner, V.F., "Reconstructing AIDS in Africa: Reply to Kaldor and Ashton", The Independent Monthly, February 1995, pp. 23-24.
81. Beral, V., Peterman, T.A., Berkelman, R.L., Jaffe, H.W. (1990), "Kaposi's sarcoma among persons with AIDS: a sexually transmitted infection?", Lancet 335:123-128.
82. Buhl, R., Jaffe, H.A., Holroyd, K.J. et al. (1989), "Systemic glutathione deficiency in symptom-free HIV-seropositive individuals", Lancet 2:1294-8.
83. Eck, H.P., 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. 370:101-8, Hoppe-Seyler.
84. Herzenberg, L.A., De Rosa, S.C., Dubs, J.G. et al. (1997), "Glutathione deficiency is associated with impaired survival in HIV disease", Proc. Natl Acad. Sci. USA 94:1967-72.
85. Montagnier, L., Olivier, R., Pasquier, C. (eds), Oxidative Stress in Cancer, AIDS and Neurogenerative Diseases, Marcel Dekker, Inc., New York, 1998.
86. 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.
87. Rosenberg, Y.J., Anderson, A.O., Pabst, R. (1998), "HIV-induced decline in blood CD4/CD8 ratios: viral killing or altered lymphocyte trafficking?" Immunol. Today 19:10-7.
88. Grossman, Z., Feinberg, M.B., Paul, W.E. (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. USA 95:6314-6319.
89. Poon, B., Grovit-Ferbas, K., Stewart, S.A., Chen, I.S.Y. (1998), "Cell cycle arrest by vpr in HIV-1 virions and insensitivity to antiretroviral agents", Science 281:266-269.
90. Ter-Grigorov, V.S., 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.
91. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M., Causer, D., Alphonso, H., Miller, T. (1999), "A critical analysis of the pharmacology of AZT and its use in AIDS", Curr. Med. Res. Opinion 15; in press.
92. Concorde Coordinating Committee (1994), "Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and deferred zidovudine in symptom-free HIV infection", Lancet 343:871-81.
93. Heresi, G.P., Caceres, E., Atkins, J.T., 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.
94. Abrams, D., "Lecture to Medical Students", Synapse, 1996.
95. Buchbinder, S.P., Katz, M.H., Hessol, N.A., O'Malley, O.M., Holmberg, S.D. (1994), "Long-term HIV-1 infection without immunologic progression", AIDS 8:1123-8.
96. Munoz, A., Kirby, A.J., He, Y.D. et al. (1995), "Long-term survivors with HIV-1 infection: incubation period and longitudinal patterns of CD4+ lymphocytes", Journal of Acquired Immune Deficiency Syndromes & Human Retrovirology 8:496-505.
97. Pantaleo, G., Menzo, S., Vaccarezza, M. et al. (1995), "Studies in subjects with long-term nonprogressive human immunodeficiency virus infection", NEJM 332:209-16; see comments.
98. Kilzer, L., "Optimistic AIDS reports beguiling at-risk men", The Rocky Mountain News, 3 May 1998, p. 3A.
99. 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.
100. Lee, T.H., Sheppard, H.W., Reis, M., Dondero, D., Osmond, D., Busch, M.P. (1994), "Circulating HIV-1-infected cell burden from seroconversion to AIDS: importance of postseroconversion viral load on disease course", J. Acquir. Immun. Defic. Syndr. 7:381-388.
101. Holodniy, M., Mole, L., Winters, M., Merigan, T.C. (1994), "Diurnal and short-term stability of HIV virus load as measured by gene amplification", J. Acquir. Immun. Defic. Syndr 7:363-8.
102. Bruisten, S.M., Reiss, P., Loeliger, A.E. 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.
103. Kaufmann, D., Pantaleo, G., Sudre, P., Telenti, A. (1998), "CD4-cell count in HIV-1-infected individuals remaining viraemic with highly active antiretroviral therapy (HAART)", Lancet 351:723-724.
104. Garrett, L. (1999), "The virus at the end of the world", Esquire 103-172.
105. Garrett, L., "AIDS, After The 'Cure': Amid setbacks, search for new hope", Newsday, Sunday 14 June 1998, p. A07.
106. Kaldor, J. and Ashton, L., "The AIDS Debate: Reconstructing AIDS in Africa", The Independent Monthly, February 1995, pp. 23-24.

About the Authors:

  • Valendar F. Turner is a Consultant Emergency Physician. He can be contacted at the Department of Emergency Medicine, Royal Perth Hospital, Perth, Western Australia, telephone +61 (0)8 9224 2662, fax +61 (0)8 9224 7045, e-mail <>, website <>.

  • Andrew McIntyre is a Melbourne-based freelance writer and social commentator. He has written extensively on the gender wars, and takes a particular interest in social and scientific issues normally avoided or distorted by the mainstream press for reasons of political expediency or cultural orthodoxy. He appears from time to time on radio and television. He can be contacted care of NEXUS.

    To Part 2

    To Part 3