Is there proof of a correlation between the "HIV" antibody and PCR tests and what may underlie such a correlation? 11 December 2003
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Eleni Papadopulos-Eleopulos,
Department of Medical Physics, Royal Perth Hospital, Western Australia, 6001,
Valendar F Turner, John Papadimitriou, Barry Page, David Causer, Helman Alfonso

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Re: Is there proof of a correlation between the "HIV" antibody and PCR tests and what may underlie such a correlation?

Is there proof of a correlation between the "HIV" antibody and PCR tests and what may underlie such a correlation?


In his rapid response “Re Perth Group responses to Christopher Noble” 27th November Christopher Noble wrote:

“Once again the 'Perth Group' have responded with an inordinate number of words but no answers.

The 'Perth Group' write: "To date we have left none of Christopher Noble's questions unanswered. The only way to prove a correlation between the antibody test and the PCR is to perform blind controlled studies. As far as we know, only one such study has been published to date."

Both of these statements are untrue.

You have previously cited several times a meta-analysis of the use of PCR in the diagnosis of HIV infection. (1) This metastudy included a total of 96 studies. Of these 11 studies (rated 3 or 4: see table 1) were found to have used blinding for both the PCR assays and reference tests. The investigators in these studies were blinded to all other tests and clinical information. The specificity of PCR for the diagnosis of HIV infection in these studies was found to be between 95 and 100%.

I have asked you several times to explain these results considering your assertion that both antibody tests and PCR tests for HIV are completely non-specific. Contrary to your assertion you have never answered this question”.


Repeat, we have answered all Christopher Noble’s questions, although maybe not always to his liking.  Let us again quote from the Owens et al analysis:


“An understanding of the diagnostic performance of PCR for HIV infection is essential in determining the appropriate role of PCR in the clinical diagnosis of such infection. However, evaluation of the performance of PCR poses difficult methodologic challenges. To evaluate the sensitivity and specificity of PCR, investigators must ascertain whether study participants are infected with HIV. Typically, a new test is compared with a superior reference (or gold standard) test…The lack of an appropriate reference test [for PCR] substantially complicates evaluation…[using the Western blot as a gold standard] We sought to 1) assess the validity and reliability of the scientific evidence on the diagnostic accuracy of PCR; 2) characterize the sensitivity and specificity of PCR on the basis of a formal analysis of the available studies; 3) develop recommendations for the clinical use of PCR in persons with suspected HIV infection; and 4) develop recommendations for the design of future studies of the diagnostic accuracy of PCR. In pursuing our third objective, we paid particular attention to whether PCR technology has improved enough to play a broader clinical role in the diagnosis of HIV infection…We assessed the appropriateness of the study design for the evaluation of the diagnostic performance of PCR on a four-point scale (1,2,3, or 4). A rating of 1 indicated that the design made the study susceptible to significant bias; a rating of 4 indicated that the study design satisfied all criteria for the evaluation of diagnostic tests Table 1”.


Two of the issues which arise from the Owen et al analysis are:

1. Is a PCR test specific for “HIV” infection?

2. Is there a correlation between a positive PCR and an “HIV” antibody test?


To claim that the PCR is specific for “HIV” infection it is absolutely necessary to:  (a) have proof that the primers originate from HIV particles.  We have repeatedly asked Christopher Noble and Brian Foley to provide references which show this is the case but so far they have failed to do so;  (b) show by the use of a gold standard that the PCR amplifies only HIV sequences and nothing else.  As Owen et al pointed out, no such gold standard exists, a view shared by one eminent “HIV”/AIDS expert, William Blattner.1


As we have already pointed out the only way to prove a correlation between the antibody test and the PCR is to perform blind controlled studies.  In the Owen et al analysis the “numbers of studies receiving a rating of 1, 2, 3, or 4 for overall study design (see Methods and Table 1) were 73, 12, 6, and 5, respectively…The criteria that were satisfied least often were adequacy of blinding during the interpretation of test results”.  The most striking feature of this meta-analysis is that of “5698 titles of potentially relevant articles” 1735 titles were judged to be potentially relevant”.  Of these only 96 met the inclusion criteria for analysis and of these only 5 (less than 0.1% of the “potentially relevant articles” had a rating of 4 which “indicated that the study design satisfied all criteria for the evaluation of diagnostic tests”.  Most importantly, although these five studies may have been blind they may not have had controls as Owens et al point out.  Thus it is not possible to state how many if any of the studies in the meta-analysis were indeed blind controlled studies.


Could Christopher Noble please tell us which of the 5 studies in the Owen et al analysis satisfied the criteria for a proper blind, controlled study or any other study apart from the one we have cited, that is, the Defer study.


The fact that Owen et al concluded:  (a) “Clearly, the performance of PCR is not adequate to justify its use as a clinical screening test”;  (b) this view is shared by many other researchers (Christopher seems to be a rare exception) and also by the CDC (see Perth Group Reponses to Christopher Noble 25th November, means that neither the specificity of the PCR nor its correlation with the antibody tests has been proven.  Even if there were a proven correlation this does not mean the positive antibody and PCR tests are the consequence of “HIV” infection.


In 1992 in Research in Immunology, an Institut Pasteur publication, we wrote:  “As long ago as 1983, one of us (E.P.-E.) proposed that oxidative mechanisms are of critical significance in the genesis of AIDS (acquired immune deficiency syndrome). A prediction of this hypothesis was that the mechanisms responsible for AIDS could be reversed by the administration of reducing agents, especially those containing sulphydryl groups (SH groups). The discovery of HIV resulted in a broadening of this hypothesis in that it considered oxidative stress as a principal mechanism in both the development of AIDS and expression of HIV”, including a positive antibody test and the appearance of any novel RNAs.2-4


If one reads Montagnier's latest writings5 and interviews6 one would be excused for concluding that Montagnier is an apologist for the oxidative and not the HIV theory of AIDS.  More than a decade after the oxidative theory of AIDS and "HIV" was proposed by our group Montagnier wrote: "A large body of data on in vitro human immunodeficiency virus (HIV) infection and biochemical clinical studies suggests that oxidative stress plays a role in AIDS pathogenesis.  Recent reports have implicated intracellular excess of reactive oxygen species (ROS) in the induction of HIV expression and in the initiation of apoptotic cell death.  Studies showing a decrease in glutathione in peripheral blood mononuclear cells from symptom-free persons offer further evidence of a metabolic alteration leading to the decreased ability to counteract oxidative stress.  In AIDS pathogenesis, oxidative stress is proposed as a metabolic alteration that favours disease progression by inducing both viral replication and apoptotic death.  Indeed, evidence that oxidative stress induces, while antioxidants inhibit, HIV replication and apoptosis suggests the use of these molecules as an antiretroviral therapy to reduce cell death in AIDS patients"7 (italics ours).


Although no mechanism is mentioned, in 2000 Montagnier accepted that novel, non-viral RNAs could arise following exposure to non-infectious agents.  At present we cannot claim proof that the positive PCR tests are the result of the oxidative stress to which the patients and cultures are exposed.  However, the fact that all the other predictions of this theory have been proven (see Addendum “Looking back on the oxidative stress theory of AIDS”8) indicates this may be the case.


Christopher Noble wrote: 

“I remind people reading this that this is an unreviewed forum. The 'articles' posted here by the Perth Group are not checked for accuracy or veracity. The BMJ has allowed the Perth Group to publish blatant lies”.


It is true that our postings may not be “checked for accuracy or veracity”.  If this is the case then the same also applies to Christopher Noble’s postings.  It is equally true that at least we have published several papers in peer reviewed scientific journals.  Given that our first paper, that which proposed the oxidative stress theory4 was published at the beginning of 1988, why has Christopher Noble not written to the editors of scientific journals questioning our interpretation of the evidence or drawing our attention to mistakes we may have made?  Why has Christopher Noble waited for 15 years and chosen a forum “not checked for accuracy or veracity” rather than availing himself of the peer reviewed process open to any scientist?

In his rapid response “0-100% specificity of the PCR test? (5th December)  Christopher Noble wrote “The Perth Group wrote: "Would Christopher Noble also please explain the 0%-100% specificity of the PCR Test?" …Unlike Christopher Noble who claims that "The metastudy however showed that PCR can be highly specific", the authors of the study reported: "When indeterminate PCR results were excluded, sensitivity ranged from 10% to 100% and specificity from 0% to 100%" and concluded "Our investigation produced two main findings. First, the false-positive and false-negative rates of PCR that we determined are too high to warrant a broader role for PCR in either routine screening or in the confirmation of diagnosis of HIV infection. This conclusion is true even for the results reported from more recent, high-quality studies that used commercially available, standardised PCR assays…We did not find evidence that the performance of PCR improved over time".11

I would like to ask the Perth Group why they have falsely quoted the meta-study by Owens et al. 1

The correct quote is "When indeterminate PCR results were excluded, sensitivity ranged from 10% to 100% and specificity ranged from 40% to 100%"”

We thank Christopher Noble for drawing our attention to this inadvertent typographical error.  We must point out that even with 40% instead of 0%, Owen et al, unlike Christopher Noble, concluded:  “…the false-positive and false-negative rates of PCR that we determined are too high to warrant a broader role for PCR in either routine screening or in the confirmation of diagnosis of HIV infection".  The question we asked Christopher Noble still stands.

Christopher Noble wrote:  “How is it possible for the Perth Group to look at the same study and make such completely different conclusions? The study contradicts their assertions that PCR and antibody testing are both non-specific.  Why is it so necessary to read the actual study rather than to simply rely on their "interpretation"? “

As Alex Russell pointed out (Re: 0-100% specificity of the PCR test?,  6th December) out unless there is proof for the existence of “HIV” all the “HIV” tests must be questioned.  Repeat, to determine the specificity of the “HIV” PCR tests it is absolutely necessary to:

(a)   have proof that the primers originated from the “HIV” particles;

(b)   have a gold standard.

Neither of these conditions have been satisfied.  This being the case, unless the most basic scientific principles are ignored the only conclusion that can be drawn by us and Christopher Noble is that the specificity of the PCR may be 100% or 0% or any number in between.



 Although lately Montagnier appears to be an apologist for the oxidative theory, at the same time he still maintains he proved the existence of HIV in 1983 and at least the principal author of the 1983 study calls “HIV” the “AIDS virus”.9  Thus could we again request Christopher Noble to please tell us whether in 1983 Montagnier discovered HIV?  Yes or no?  If yes what is the evidence in Montagnier’s paper “that a virus, later called HIV, can be found in patients that have AIDS”?  What is the evidence in his 1983 paper that such a virus exists in anyone?




1. Blattner WA. Retroviruses. In: Evans AS, editor. Viral infections of humans. 3rd ed. New York: Plenum Medical Book Company, 1989:545-592.

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

3. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Is a positive Western blot proof of HIV infection? Biotechnology 1993;11:696-707.

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

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

6. Passwater RA. Antioxidant Nutrients and AIDS: Exploring the Possibilities--An interview with Dr. Luc Montagnier, the discoverer of HIV. Whole Food Magazine, 1995:50-65.

7. Piedimonte G, Guetard D, Magnani M, Corsi D, Picerno I, Spataro P, et al. Oxidative protein damage and degradation in lymphocytes from patients infected with human immunodeficiency virus. J Infect Dis 1997;176(3):655-64.

8. Papadopulos-Eleopulos E. Looking back on the oxidative stress theory of  AIDS. Continuum 1998;5 (5):30-35.

9. Barre-Sinoussi F. Historical accuracy of HIV isolation-Reply. Nat Med 2003;9:1235-1236.





This article is also at


The article upon which it is based (Reference 4 above) is at





Eleni Papadopulos-Eleopulos

Department of Medical Physics

Royal Perth Hospital


Western Australia

Published in Continuum Magazine Volume 5 No. 5 1998/99.  Pages 30-35



The whole-purpose of a scientific theory is to explain the mechanism behind observations and make predictions.  If a theory cannot explain the observations for which it was put forward, or if its predictions are not fulfilled, then it should be abandoned.  In this regard, despite the lapse of 18 years, there is still no proof as to the cause(s) of AIDS.  Of course, there are theories but the biggest obstacle in overcoming the problem of AIDS, and proving its cause, is that one of these theories, the HIV theory, has been uncritically accepted since 1984.  However, of all the theories, the HIV is the least likely.


The observations the HIV theory was proposed to explain were threefold.  The high frequency of a malignancy, Kaposi’s sarcoma (KS), a few opportunistic infections (0I), principally Pneumocystis carinii pneumonia, and a decrease in a specific cell type, T4 lymphocytes, in gay men, IV drug users and haemophiliacs.  It was accepted that no single infectious agent could possibly be the direct cause of the multiple diseases seen in AIDS patients.  So, it was proposed that the "hallmark" of HIV infection was the destruction of T4 cells by HIV which inevitably led to the appearance of KS and the OI.  The proposition that decrease in T4 cells was the hallmark of HIV/AIDS is difficult to comprehend.  At the time when the HIV theory of AIDS was put forward

(a)               there was no evidence that retroviruses kill cells, to the contrary;

(b)               many factors to which patients belonging to the AIDS risk groups are exposed are immunosuppresive.


This fact was known to some of the best known HIV experts.  In 1985 Montagnier wrote: "This syndrome [the AIDS diseases] 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.1 In the same year Weiss, Ludlum and their associates wrote (concerning patients with haemophilia): "Our finding supports our previous conclusion that the abnormal T-lymphocyte subsets are a result of the intravenous infusion of Factor VIII concentrates per se, not HTLV-III infection".2  One year later researchers from CDC.  "...factor concentrate [Factor VIII] itself may be immunosuppresive even when produced from a population of donors not at risk for AIDS"3

(c)        evidence also existed that many factors including infections, and trivial ones, such as exposure to the sun or radiation in solaria lead to decreased T4 cells.  Although some of the T4 decreases were long lasting, the patients did not develop KS and OI, a significant proportion of the "AIDS" patients, including patients with KS and 0I infections, had normal numbers of T4 cells.  In other words, T4 decrease (immune deficiency) is neither necessary nor sufficient for the development of KS and 0I.  Thus the proposition that KS and the 0I are the result of T4 decrease and that the T4 decrease detected in the patients belonging to the AIDS risk groups was caused by HIV infection was totally inconsistent with the data available even before the hypothesis was put forward.  For some time now, all HIV/AIDS experts, including Robert Gallo, accept that HIV has no direct or indirect role in KS.5-7



The HIV theory predicted that HIV was sexually transmitted and therefore AIDS would spread throughout the heterosexual population.  Obviously this has not happened.  The prediction by proponents of the HIV theory that a vaccine would be developed by 1986 also has not been fulfilled.  In 1984 Montagnier said that the only way to prove HIV is the cause of AIDS is to have an animal model.8  Although no effort has been spared, no model of a retrovirus causing AIDS has been forthcoming.  Indeed, the only animal model that bears any resemblance to human AIDS fully supports a non-infectious modus operandi.9



At the outbreak of AIDS, Gallo had already spent a decade in attempts to prove that the cause of some cancers was a retrovirus.  This led him to put forward the retroviral theory of AIDS.  From an equally biased position I put my non-infectious theory.  Although trained as a nuclear physicist, with the exception of a few years, I have worked in the medical field in the Department of Medical Physics of the Royal Perth Hospital, the largest teaching hospital in Western Australia.  Among its many activities it was involved in treating cancer by radiation and pioneered hyperthermia for the same purpose.


It was known that both radiation and radio-sensitisers were oxidising agents, and apart from hyperbaric oxygen the chemical radiosensitiser included compounds containing the -NO2 group, that is, nitro-compounds.  To understand the interaction between the agents used to treat cancer and cancer tissue, I first needed to determine what makes a cell cancerous.  I decided the best way to approach this was to attempt to fully understand the normal cell.  This included the understanding of the mechanism by which sperm induced the division of the ova.  In doing so I developed my own theory of biological functioning.  A short version was first presented at a meeting in Colorado in 1979 and was published in Speculation in Science and Technology in 1980.  A more detailed version was published in 1982 in the Journal of Theoretical Biology, after it was first rejected by Nature, under the title "A Mitotic Theory".  Although the title suggests that it deals only with cellular division and cancer, the theory, as one of the reviewers pointed out, also proposed a "relationship between modifications in the redox state of the actin-myosin system and other key biological processes (e.g. transport, muscle function, metabolism). Most importantly in this article, there is a clear integration of older and present data as well as "classical" and "contemporary" concepts.


The theory claimed that the cellular redox level and its oscillations, that is, the cyclic variation between oxidation and reduction, plays a pivotal role in both normal and abnormal cellular function and structure.  Diseases such as cancer, cardiovascular, clotting abnormalities and ageing, for example are the result of perturbation of the cellular redox level and its oscillations.


Thus, by the time AIDS was diagnosed, I was aware of the biological and pathological effects induced by many agents (semen, nitrites, recreational drugs, Factor VIII, infectious agents and the drugs used to eradicate them) to which the patients belonging to the AIDS risk groups were exposed.  More importantly all these agents showed a common property, they were oxidising agents.  This led me to put forward the non-infectious theory of AIDS which claimed that the primary risk factors for AIDS were the oxidising agents to which the individuals were exposed.  While the manuscript discussing this theory (in which neither HTLV-I nor Montagnier's retrovirus were mentioned) was in the hands of a few colleagues for evaluation, Gallo claimed to have proven that HTLV-III was the cause of AIDS.  I was advised to re-write the manuscript to take account of these claims.  The revised manuscript, which was twice rejected by Nature and initially by Medical Hypotheses, was later accepted by the latter journal.



The predictions of my theory included.


(1 ) AIDS would remain restricted to the risk groups.

This has been the case.

(2) The only sexual act leading to AIDS or a positive antibody test is a very high frequency of receptive anal intercourse in either sex.  One of the first to publish supporting evidence of this was Gallo and his associates.  In a study published in 1984 he wrote.  "of eight different sex acts, seropositivity correlated only with receptive anal intercourse and was inversely correlated with insertive anal intercourse".10  In 1986 Gallo wrote, "Data from this and previous studies have shown that receptive rectal intercourse, for example, is an important risk factor for HTLV-III [HIV] infection.  Yet, at the time of entry into this project, nearly half of the participants still practised this technique.  We found no evidence that other forms of sexual activity contributed to the risk".11 Thus Gallo was one of the first to publish evidence which contradicted his own assertion that HIV/AIDS is bi-directionally sexually transmitted.


In 1985 Montagnier and his colleagues reported that the wife of a haemophilia man who, in addition to other sexual acts, practised anal intercourse was found to have a positive antibody test and low numbers of T4 cells.  "During 10 months of follow-up his wife remained clinically well, discontinued exposure to semen, and then lost the LAV antibody, and regained a normal number of T-helper cells" (T4 cells).12


The best and largest study, the Multicenter AIDS Cohort Study of 4995 gay men, which commenced in 1984 and is ongoing, also confirmed this in 1987.  "Receptive anal intercourse accounted for nearly all new HIV infections among the homosexual men enrolled in this study, and the hazards of this practice need to be emphasised in community educational projects".13


In a review of most, if not all, epidemiological studies conducted in gay men published in 1994, the authors concluded.  "it can be said that the cited reports yield convincing evidence that (1) unprotected ano-genital receptive intercourse poses the highest risk for the sexual acquisition of HIV-1 infection.' (2) ano-genital insertive intercourse poses the highest risk for the sexual transmission of HIV-1 infection. (3) there is mounting epidemiologic evidence for a small risk attached to oro-genital receptive sex, biologic plausibility, credible case reports and some studies show a modest risk, detectable only with powerful designs. (4) sexual practices involving the rectum and the presence of (ulcerative) STD facilitate the acquisition of HIV-1. (5) no or no consistent risk for the acquisition of HIV-1 infection has been reported regarding other sexual practices such as ano-genital insertive intercourse and oro-anal sex... (8) the association of substance use with HIV infection is probably the result of interaction, because substance use increases the likelihood of practising ano-genital receptive intercourse".14


Unquestionably, to date, the best designed and executed study in heterosexuals was conducted by Nancy Padian and her associates.  In a paper entitled "Male-toFemale Transmission of Human immunodeficiency Virus" published in 1987 wrote: " The total number of exposures to the index case (sexual contacts with ejaculation) and the specific practice of anal intercourse, also with the infected partner, were associated with transmission”.15  The results from their long prospective study of couples, of whom only one partner of either sex was antibody positive, were published in 1997 in a paper entitled Heterosexual Transmission of Human Immunodeficiency Virus (HIV) in Northern California,. Results from a Ten Year Study.


"Prospective results.

We followed 175 HIV-discordant couples over time, for a total of approximately 282 couple-years of follow-up...At last follow-up, couples were much more likely to be abstinent or to use condoms consistently, and were much less likely to practice anal intercourse (p < 0.0005 for all).  Nevertheless, only 75% reported consistent condom use in the 6 months prior to their final follow-up visit... no seroconversions occurred among exposed partners".16


Thus, a positive antibody test and AIDS, like pregnancy, can be sexually acquired but not sexually transmitted.  The difference is, that while pregnancy can be acquired by a single sexual intercourse, for AIDS to appear a very high frequency of receptive intercourse over a long period is absolutely necessary.  AIDS is more like cervical cancer.  The effect is not the result of the act itself, but its high frequency.  But, as with pregnancy and cervical cancer, other factors may mitigate against the development of AIDS.


(3) Both antibody positive and antibody negative drug users will develop AIDS and that not only individuals who use dirty needles but also those who use clean needles or even non-parenteral drugs will develop positive antibody tests.


According to an interview published in the June 1986 issue of AIDS ALERT with Susan Neshin, Medical Director of Asbury Park (NJ) Drug Treatment Center, for clinicians to differentiate between AIDS and the health problems typically experienced by intravenous drug users, "First clinicians should interview NDUs to determine if their symptoms are related to drug abuse or AIDS.  You have to talk to them and get them to tell you if their symptoms are drug-related.  They can have weight loss, diarrhoea, and night sweating, but they could be having that on an ongoing basis from bad dope. withdrawal, or just poor health in general.  It's very common for drug addicts to have inguinal lymphadenopathy, and maybe a few cervical or axially nodes that are kind of shotty.  If you see oral candidiasis in an NDU, that's a real tip off".  A few months later researchers from the USA wrote, "a real T- helper lymphopenia [that is, T4 cell decrease] is only consistent with and not diagnostic of AIDS;  other diseases and some treatment regimens also can express a T-helper lymphopenia. such as hospitalised IV drug abusers”.17


One year later, in an article published in the British Medical Journal, one reads, "Intravenous drug abusers appear to be at special risk of acquiring tuberculosis, and a high rate of infection in this group was reported well before AIDS began".18


In a 1994 paper published in the Scientific American, two researchers who studied drug abuse wrote, "Many manifestations of AIDS in drug users who inject are quite different from those in homosexual and bisexual men who do not use drugs in this manner; in drug users who inject and in their sexual partners HIV infection is associated with substantially increased morbidity and mortality from bacterial infections.  In the US much of the resurgence of tuberculosis is occurring among HIV-infected users who live in crowded conditions without access to good medical care.  The CDC definition of AIDS has been periodically updated to incorporate these findings".19


In 1994, researchers from Switzerland reported their findings from a prospective study designed "to examine differences in the incidence and spectrum of diseases comprising 314 HIV-seronegative NDU, 217 HIV-seropositive NDU, and 10 NDU with admissions registered in either group (from a total of 1011 admissions)".  Narcotic drug users (NDU) were enrolled in the study if "they were hospitalised for a minimum of 24 hrs, and also presented with at least one of the following characteristics: history of either parenteral drug use or a corresponding oral substitutive medication (mainly methadone). or actual intoxication and miosis [pinpoint pupils] responding to naloxone. or opiate or cocaine metabolises in a urine sample.  Individuals with exclusive oral drug use other than opiates were not included".  "HIV-seropositive NDU were more frequently admitted for infectious complications or various non-infectious medical complications (including as most frequent cases, 38 admissions for ill-defined episodes, 11 for repeated seizures, nine for acute pancreatitis, and six for adverse medical drug reaction).  Moreover, they also tended to have a higher admission incidence density for intoxication, whereas there was no difference in admissions for suicide tentative or withdrawal reaction".  However, individuals from both groups, seropositive and seronegative were admitted for "infectious complications", including non-opportunistic pneumonia, purulent bronchitis, tuberculosis, soft tissue infection, osteoarticular infection, endocarditis, primary bacteremia and disseminated candidiasis.  More importantly, of a total of 541 admissions of seropositive individuals, 187 (35%) were individuals who had an ORAL mode of drug "application" and 9 (0.5%) inhalation".20


That both intravenous and oral drug users develop positive "HIV" antibody tests was shown as far back as 1988 when Sterk reported that a higher percentage of prostitutes who use oral drugs (84%), than IV (46%), test positive”.21


In another study published in 1993, researchers from New York City tested 1246 seronegative drug users.  "Nine had at least one CD4 cell count of <300 cells/ul or a CD4<20%" and 21 subjects "had one CD4 cell count between 300 and 500 cells/ul".  They also reported that "CD4 cell counts of <500 cells/ul were, however, associated with subsequent HIV seroconversion…The relative risk for seroconversion among subjects with one or more CD4 count <500 cells/ul, compared with HIV-negative subjects with ail counts >500 cells/ul was 4.53...consistent with an Italian study showing IDUs with CD4 counts <1,000/ul were more likely to seroconvert".22  (The authors of the latter reported a "low number of T4 cells was the highest risk factor for HIV infection" (relative risk=8.5)23.  In other words, in drug users, a decrease in T4 cells instead of following seroconversion is a predictor for seroconversion, a finding completely at odds with the HIV theory of AIDS.


(4)        In Africa there was neither a new disease AIDS nor a new virus HIV.  When Reappraisal of AIDS:  Is the oxidation caused by the risk factors the primary cause? as finally published was written in 1984/85, Africa was not considered an important issue.  Thus, Africa is only briefly mentioned.  Following the 1986 Paris AIDS conference, AIDS in Africa became the defining example of heterosexual transmission.  This is the reason that my paper was initially rejected by Medical Hypotheses.  The March 1987 letter of resubmission was accompanied by a 12 page document entitled "AIDS in Africa and its heterosexual transmission".  This included the following summary:



a.       The operational definition of AIDS in Africa is different from the rest of the World.  In Africa there is neither direct or indirect data which proves beyond any scientific doubt the existence of a new disease, AIDS, which affects both men and women equally and of its postulated causative virus, HTLV-III/LAV assumed to be sexually transmitted.


b.       In Africa immune deficiency, opportunistic infections and KS exist and have existed for a long time in both men and women.  However the pathogens could be other than HTLV-III/LAV, for e.g. poverty, infections other than HTLV-III/LAV and the drugs used for their treatment, copper, recreational drugs (if not opiates other traditional drugs), anally or orally deposited sperm itself via homosexual, bisexual or heterosexual practices.


The data from Africa used to prove heterosexual transmission will not stand up to even superficial scientific analysis".


The detail of the text included.



In 1, Piot et al., [Lancet 1984, 2: 65] found that 7 out of 12 controls had low T4 /T8 ratio, 5 of which were due to a decreased T4.  They state "Tuberculosis, protein caloric malnutrition and various parasitic diseases can all be associated with depression of cellular immunity".


"…Among healthy Africans resident in a non-AIDS area, the number of helper and suppressor lymphocytes were the same in HTLV-III/LAV seropositive and seronegative subjects... (Bigger, Lancet 1986, 1, 79).


" Parasitic diseases and malnutrition are two possible causes of immunodepression in Africa.  A wide range of prevalent protozoal and helminthic infestations have been reported to induce immunodeficiency" (Clumeck, JAMA, 1985,254,2599).


" Mild sunstroke induces immunosuppression including T4/T8 inversion" (Walker, Lancet, 1983, 2, 344).


"Normal volunteers (hospital and university staff) underwent a 12 half-hour exposure to a commercially available solarium on consecutive days excluding Saturday and Sunday, to acquire a suntan.  Tests of immune function were carried out before, on completion and 2 weeks after exposure.  A number of abnormalities were found in the exposed subjects including significant decrease in T4 and T4/T8 which persisted 2 weeks after exposure". (Hersey, Lancet, 1983, 1, 545).



Very high levels of HTLV-III/LAV seropositivity has been reported from Africa.


"…25% of a sample of hospital workers in Zaire were seropositive in 1984" (Frazer, Med.  J. Aust 1986, 145, 525).


" 65% of Ugandan children were found to have been positive in 1972" (Gallo etal., Ann.  Int.  Med. 1985, 103, 679).


"15.5% of blood donors were found to be positive at Kigali in Rwanda in 1984" (Clumeck, JAMA, 1985, 254, 2599).


"41 out of 410 (10%) of healthy medical personnel from Mulago Hospital Kampala were positive for HTLV-III/LAV. 5 out of 30 (17%) of controls outside the hospital were positive. 4 out of 10 (40%) of control patients deemed sexually immature were also found positive" (Serwadda, Lancet, 1985, 2, 849).


"Of a total of 274 patients at the Makala Tuberculosis Sanatorium in Kinshasa, half of the suspected pulmonary cases (total 56); one third of the confirmed pulmonary cases (160) and two thirds of the remaining 15 who were confirmed to have extrapulmonary disease tested positive both in the ELISA and Western blot." (Mann, Paris Conference).


"Forty out of 368 (11%) children admitted to Mama Yemo Hospital in Kinshasa, Zaire were positive by ELISA and 39 out of the 40, also by Western Blot.  Clinically seropositivity was associated with the diagnosis of malnutrition and pneumonia" (Davachi, Paris Conference).


"21 % of the staff at the Zambian Consolidated Copper Mines, and 14% of males and 44% of females at the mine hospital were found positive.  Other people tested who had no connection with the mines were negative." (Buchanan, Lancet, 1986, 1, 155)


The diversity of these reports leads to the conclusion that, either copper mining, tuberculosis, malnutrition and pneumonia have as their aetiological factor HTLV-III/LAV or the tests are non-specific.  If the tests are specific, because 10-30%. of infected cases develop AIDS within 3 years (Bigger, Lancet, 1986, 1, 79) then 1.5-4.6% of the Rwanda population (certainly of its blood donors) and 3.5-7.5% of the Zaireans (certainly of the medical staff at the hospital where the tests were done in 1984) should be either dead or dying by the middle of this year, not to mention prostitutes, Ugandan children, TB patients and workers in regions with copper mining.  Obviously this is not the case.  Even Quinn Mann, Curren and Piot admit that in developing countries, "...serodiagnosis is complicated by the need for confirmatory testing because of the presence of possible cross-reacting antibodies" (IV). (Quinn et al., Science 1986, 234..955)


The final section examined the evidence for heterosexual transmission of AIDS in Africa and concluded that "we are left with a sexually transmitted disease which:


(a) Has continental preferences

(b) Has racial preferences

(c) Has sexual preferences.  The same bisexual men can get infected by an African woman but not by a confirmed homosexual AIDS patient with whom he practices repeatedly exclusive active intercourse".


That even today in Africa there is no such thing as a new disease AIDS, and that a positive antibody test does not prove HIV infection, it suffices to mention that:  according to an editorial in the July 11th 1998 Lancet, the developing world "bears more than 90% of the global burden of HIV infection" and "Tuberculosis (TB) is the leading cause of death worldwide among people with HIV";  no less an authority in AIDS in Africa than de Cock admits that TB has been present in Africa in endemic proportions long before the AIDS era";24  no less an authority on HIV/AIDS than Essex has proved that in Africa a positive antibody test does not prove HIV infection".25


(5)        The theory also predicted that decrease in T4 cells is not the hallmark of either HIV infection or the clinical syndrome, that is, the decrease in T4 cells is not HIV specific and is neither necessary nor sufficient for the syndrome to appear, that is, the clinical syndrome is not the result of immune deficiency.  In fact it was postulated that the decrease in T4 cells may not be due to their destruction by HIV or any other agent but could result from (i) the extreme sensitivity of T cells to oxidative stress;  (ii) T4 cells possessing a lower negative charge than T8 cells could be the first to be destroyed by persistent oxidative stress; (iii) T-cells sequestrated in diseased peripheral tissues;  (iv) decreased binding of the T4 antibody as a result of changes in their surface, that is, due to "down regulation" of the CD4 receptor.  To illustrate that at present this is accepted even by HIV/AIDS experts it suffices to quote three papers published last year and one more recently:


"This article discusses the importance of alterations in the CD4+ and CD8+ cell migration in regulating blood lymphocyte levels and questions the extent of virus mediated CD4+ cell destruction".26

 "Along with other recent analyses and experimental developments these considerations also suggest a need to re-evaluate current concepts about HIV pathogenesis, including the concept that a systemic depletion of CD4, T cells is the hallmark of the disease".27

"CD4+ T-cell lymphopenia is due to both shortened survival time and a failure to increase the production of circulating CD4+ T-cells.28


(6)        A most important prediction was that the tissues of AIDS patients and those at risk would be oxidised, in general, and in particular they would have low sulphydryl (-SH) group levels.  In recent years there have been hundreds of papers confirming this prediction.  The first was published by German researchers who, for reason(s) not stated, undertook experiments to determine the level of reduced thiols (-SH) in the blood of "HIV" infected individuals.  They found that.  "Blood plasma samples from HIV-1 infected persons contain elevated glutamate concentrations up to 6-fold the normal level and relatively low concentrations of acid-soluble thiol (i.e. decreased cysteine concentrations).  The intracellular glutathione concentration in peripheral blood-mononuclear cells (PBMC) and monocytes from HIV antibody-positive persons are also significantly decreased.29   Last year a book published with Luc Montagnier as principal editor further confirms the involvement of oxidative stress in AIDS.30


(7)        The 10th of July 1986 letter of re-submission to Nature was accompanied by a response to the reasons given by the Journal for rejection.  The response ended with the following.  "If my paper does nothing other than draw attention to the oxidative nature of the risk factors and its biological importance, then it offers what is so far the only hope of treatment which will arrest and reverse the otherwise invariable fatal course of the disease.  In my opinion this alone would more than justify its publication".


Indeed the most important practical prediction of the theory was that AIDS can be prevented and treated by stopping exposure to the oxidising risk factors and by using "currently available therapeutic [antioxidants in general and SH-containing, in particular] substances".  The best confirmation of this comes from researchers at Stanford University, USA.  In 1997 discussing their results they wrote:  "In essence, we have shown that GSH levels are lower in subjects with CD4 T cell counts below 200/ul (CD4 <200) than in subjects at earlier stages of HIV disease;  that among subjects with CD4 <200, lower levels of GSB (a FACS measure of GSH in CD4 T cells) predict decreased survival.' and that the probability of surviving 2-3 years increases dramatically as GSB levels approach normal range.  In addition, we have presented preliminary evidence suggesting that oral administration of NAC, which supplies the cysteine required to replenish GSH, may be associated with improved survival of subjects with very low GSH levels" (GSH-reduced glutathione)".31


Last year they stated: "We have shown that GSH depletion is associated with impaired survival., the greater the depletion, the worse the prospects for survival By replenishing GSH.  NAC or other agents we may be able to modulate such adverse effects of GSH depletion".30  However, although the authors are most probably aware of our work (the publications of the Perth group were sent to them a few years ago and are indexed in the MEDLINES under oxidative stress), for some unknown reason, they state:  "HIV-infected individuals would be better served if we could identify the mechanism that underlines the GSH depletion and intervene, it possible, to prevent its occurrence".  The best advice they can give in this regard is: "it may be prudent for those individuals to avoid excessive exposure to UV irradiation and unnecessary use of drugs that can deplete GSH- e.g., alcohol and prescription or over-the-counter formulations containing acetominophen [paracetamol]".


(8)        Perhaps the boldest claims and predictions were made regarding the existence of HIV.  I wrote HIV, "has never been isolated from fresh AIDS tissues".  Furthermore, HIV "has never been isolated as an independent stable particle".  That is, HIV had not been isolated from either fresh tissues or culture, which means that its existence had not been proven and this situation has not changed up to the present day.  At least Montagnier in his 1997 interview to Djamel Tahi admitted that he had not isolated HIV and in his view neither had Gallo.32  I presented evidence that the observed phenomena (particles, reverse transcriptase, antibody/antigen reactions) which were said to prove the existence of HIV were not specific to a specific retrovirus nor even to retroviruses in general.  Unlike Gallo, Montagnier when interviewed by Djamel Tahi, eventually reluctantly admitted that these phenomena were not retrovirus specific.


I cited examples of evidence which, taken together, led to the conclusion that oxidising agents were causing not only AIDS but also gave rise to the phenomena which were interpreted by the Montagnier and Gallo school as indicating the presence of HIV.


As far back as 1986 Montagnier knew that the phenomena could not be obtained unless the cultures were stimulated, although he did not know that the stimulants were oxidising agents.33  In 1991 Anthony Fauci proved that the "H IV" phenomena could be inhibited by antioxidants.34



It is over twenty years since I conceived the redox theory of cellular function and nearly as long since its specific application to the problem of AIDS appeared in Medical Hypotheses.  I look back over this time with very mixed feelings.  Naturally I am proud that as a scientific theory every prediction concerning AIDS has materialised.  However, I am saddened that there are forces at work which have consistently prevented purposeful but friendly debate.  To me and my group the problematic nature of the HIV theory was apparent from the very beginning.  It is now my fervent hope that, as the HIV theory continues to fail the many patients who are diagnosed with antibodies to "HIV" and AIDS, the time is rapidly approaching when scientists and physicians will be eager to examine our contribution.



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2.         Ludlam CA, Steel CM, Cheingsong-Popov R, et al. Human T-Lymphotropic Virus Type-III (HTLV-III) Infection in Seronegative Haemophiliacs after Transfusion of Factor VIII. Lancet 1985;ii:233-236.

3.         Jason JM, McDougal JS, Dixon G, et al. HTLV-III/LAV Antibody and Immune Status of Household Contacts and Sexual Partners of Persons with Hemophilia. JAMA 1986;255:212-215.

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

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

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

7.         Lauritsen J. NIDA Meeting Calls for Research into the Poppers-Kaposi's Sarcoma Connection. The New York Native 1994:At website

8.         Vilmer E, Rouzioux C, Vezinet Brun F, et al. Isolation of new lymphotropic retrovirus from two siblings with Haemophilia B, one with AIDS. Lancet 1984;i:753-757.

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

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virus. JAMA 1987;258:788-90.

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19.       Des Jarlais DC, Friedman SR. AIDS and the use of injected drugs. Sci. Am. 1994:56-62.

20.       Scheidegger C, Zimmerli W. Incidence and spectrum of severe medical complications among hospitalized HIV-seronegative and HIV-seropositive narcotic drug users. AIDS 1996;10:1407-14.

21.       Sterk C. Cocaine and HIV seropositivity. Lancet 1988;i:1052-1053.

22.       Des Jarlais DC, Friedman SR, Marmor M, et al. CD4 lymphocytopenia among injecting drug users in New York City. J. Acquir. Immun. Defic. Syndr. 1993;6:820-822.

23.       Nicolosi A, Musico M, Saracco A, Molinari S, Ziliani N, Lazzarin A. Incidence and risk factors of HIV infection: A prospective study of seronegative drug users from Milan and Northern Italy, 1987-1989. Epidemiology 1990;1:453-459.

24.       De Cock KM, Soro B, Coulibaly IM, Lucas SB. Tuberculosis and HIV infection in sub-Saharan Africa. JAMA 1992;268:1581-7.

25.       Kashala O, Marlink R, Ilunga M, et al. 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. 1994;169:296-304.

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Competing interests: None declared