The Predictions of the "HIV" and Oxidative Theories of AIDS 22 March 2005
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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, Sam Mhlongo, Todd Miller, Christian Fiala

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Re: The Predictions of the "HIV" and Oxidative Theories of AIDS



It is accepted that a theory is as good as its predictions.


The predictions of the "HIV" theory of AIDS

 When we have asked Nicholas Bennett to tell us which were the main predictions of the "HIV" theory of AIDS he replied (Re: Oxidation - the primary cause of AIDS and "HIV"", 22 January: 


1.                  "HIV serology should precede AIDS".  If "HIV" is the cause of AIDS then the first prediction should be: "HIV should precede AIDS".  This can be paraphrased as "HIV serology should precede AIDS" only if evidence exists that the antibody tests are "HIV" specific.


We have always maintained that a positive antibody test predicts the presence of future development of pathology including the diseases which are said to indicate AIDS. The question is “Do these antibody tests prove “HIV” infection?” Neither Nicholas Bennett nor Peter Flegg nor Brian Foley nor anybody else has given any evidence to support “HIV” infection.

In his latest effort to justify the “HIV” Western Blot test, (“HIV tests”, 26 January 2005) all Nicholas Bennett could give answering Rob McGregor (Re: Re: Oxidation – the primary cause for AIDS and “HIV””, 25 January 2005) was: “The differences in Western Blot criteria again boil down to differences in the test kits used. Each kit is developed differently - some using recombinant proteins, some using virus preps, some using peptides. It makes sense that depending on the specific antigen being presented and the mode of presentation, sensitivity and specificity for individual bands will vary. This is why each kit includes appropriate interpretation instructions, again based upon comparisons with standardised panels.”

It is true that the test kits may contain different antigens. However, it is also true, and surely Nicholas Bennett is aware of this, that one and the same kit is used in different countries and different laboratories with different criteria of interpretation of the results based upon different “standardised panels”. Furthermore, these “standardised panels” and the criteria for a positive test have been introduced arbitrarily. Surely Nicholas Bennett is aware that the specificity of the “HIV” antibody tests can be determined only by comparing the results of the antibody tests with the presence or absence of “HIV”. (The presence or absence of “HIV” must be determined by a method which does not involve antibody-antigen reactions, namely “HIV” isolation).


To date nobody has presented such evidence.[1]  To the contrary.  "While serodiagnosis is now used routinely for demonstrating exposure to HIV, none of the tests currently used is able to differentiate perfectly between infected and uninfected individuals".[2] There are many such statements in the HIV literature some of which have been documented by UK investigative journalist Neville Hodgkinson in his article “ Why an HIV test may not provide proof positive at all. The critical flaws in the methods we use to detect the killer virus” published in The Business May 2004 HERE (search the page for “Thomas Zuck”). 


We have repeatedly mentioned in this debate that our claim that the specificity of the "HIV" antibody test has not been determined (no gold standard exists) has been accepted by some of the best experts in HIV testing, including Mortimer and Blattner, as well as antibody test kit manufacturers.


2.                  "HIV serology should predict HIV detection via other means (e.g. culture, PCR, antigen testing)"


Repeat:  "In the antibody tests, the "HIV" proteins are given and are reacted with sera containing antibodies.  When a reaction takes place, the reacting antibodies are said to be "HIV".


In "culture" and "antigen testing", the "HIV" antibodies are given and are reacted with either the culture contents or with antigens.  If a reaction takes place, then it is claimed proof for "HIV isolation" or detecting of "HIV" proteins.  (See the very often cited papers by David Ho or Brooks Jackson).


Since it is the same reaction involved in the three tests, it is likely that some correlation is found between them.


We have repeatedly asked Nicholas Bennett to give us a few references in which the specificity of the PCR for "HIV" has been proven".  Nicholas Bennett has never responded to our request.


In fact, no correlation exists between "serology", "culture", "PCR" and "antigen testing".[3 4]


See also “The isolation of HIV - Has it really been achieved?”


Furthermore and most importantly, even if a correlation between all these tests did exist, since there is no evidence that even one of them is specific to "HIV", it is difficult to see how Nicholas Bennett's second predictions will add credit to the "HIV" theory of AIDS.


3.                  "Pharmacological intervention against the virus should inhibit the viral replications in vitro and in vivo, and result in restriction of the immune dysfunction seen in AIDS and pre-AIDS complex patients".


The most often used method to determine "viral replication", is "viral load".  We asked Nicholas Bennett "to give us a few references where it has been shown that "viral load" means "HIV" infection and that a decreased "viral load" means inhibition of "HIV" replication".  No such references have been given to us.  In fact all the "HIV" experts (including the CDC's) as well as "viral load" test kit manufacturers concur that "viral load" cannot be used to prove "HIV" infection.

Again, given the fact that no evidence exists that the "viral load" test means "HIV" RNA, it is difficult to see how it's inhibition by "pharmacological intervention", that is Nicholas Bennett's third prediction, will lend weight to the "HIV" theory of AIDS.


4.                  "HIV" serology should, obviously, appear to be transmissible and associate with the individuals and risk groups with AIDS".


Let us repeat.  The main mode of "HIV" transmission is said to be sexual and the main risk groups in the developed countries to be gay men.  Let us once again remind Nicholas Bennett that bi-directional transmission is required for an agent to be sexually transmitted.  In a previous rapid response we drew attention to the following facts.  In 1984, Robert Gallo and his colleagues wrote "Of eight different sex acts, seropositivity correlated only with receptive anal intercourse….and with manual stimulation of the subject's rectum (receptive "fisting")….and was inversely correlated with insertive anal intercourse."  Two years later they confirmed their 1984 findings:  "In this analysis, only receptive rectal intercourse, douching, rectal bleeding…were significant predictors (p<.05) of anti-HTLV-III positivity…We found no evidence that other forms of sexual activity contributed to the risk."  In a 1994 review of all the major studies conducted in gay men including the longest, largest, best-designed and executed published study of gay men anywhere in the world, the MultiCenter AIDS Cohort Study, the authors concluded:  "(1) unprotected anogenital receptive intercourse poses the highest risk for the sexual acquisition of HIV-1 infection;  (2) anogenital 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 orogenital receptive sex,…(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 anogenital insertive intercourse and oroanal sex…".


Since the main and absolutely necessary property of sexually transmitted agents is bidirectionality, that is, transmission from the passive to the active partner and vice versa, this means "HIV" cannot be sexually transmitted.  In other words, "HIV serology" like pregnancy, is sexually acquired but is not sexually transmitted.


For more than 20 years the "HIV"/AIDS experts have been claiming that humans are infected with a bi-directionally sexually transmitted virus, "HIV", and that by now more than 50 million individuals have been infected by this mode.  Yet, incredibly the only reference Nicholas Bennett could provide for a bi-directional transmission of "HIV serology" is a paper on murine (mice) retroviruses.


For some unknown reason Nicholas Bennett failed to mention three of the main predictions of the "HIV theory of AIDS.  Namely:  (a) "HIV" and thus AIDS would spread throughout the heterosexual population in the USA, Europe and Australia.  This has not happened.  The prediction that a vaccine would be developed by 1986 has not been fulfilled.  Even today no such vaccine exists or is likely to in the foreseeable future.

In 1984 Montagnier said that the only way to prove HIV is the cause of AIDS is to have an animal model.  According to Dr. Joseph L. Bryant, Director of the Animal Models Division at Gallo’s Institute of Human Virology, Baltimore, "To my knowledge, almost all major scientific successes on unraveling and conquering human diseases has been with the use of animal models. AIDS and AIDS-associated diseases will be no exception." Although no effort has been spared no model of an "HIV" AIDS animal model has been forthcoming.  In fact the only AIDS animal model to date supports the oxidative theory of AIDS.[5]


In conclusion, at present no evidence exists to support the predictions of the "HIV" theory of AIDS.  In fact the "HIV" theory cannot even account for the two main phenomena for which it was put forward, KS and T4 cell decrease and thus the opportunistic infections.  At present it is accepted that the cause of KS is not "HIV".  The "discoverers" of "HIV", Montagnier and Gallo, have shown that "HIV" does not kill the T4 cells.[6-8]


In fact, according to Montagnier the decrease in T4 cells precedes, does not follow, "HIV" infection[9] and the T4 cell death is by apoptosis caused by oxidation.[10]


In conclusion, at present no evidence exists to support the predictions of the “HIV” theory of AIDS.   


The cornerstone of the “HIV” theory of AIDS is:

(i)                  “HIV” kills the T4 cells (AID).

(ii)                The decrease in T4 cells causes the clinical syndrome (S).


But, according to Nicholas Bennett (“HIV mechanism revisited”, 2 October 2005):


(i)                  “What is important is that HIV can induce a decline in CD4 counts, not that all low CD4 counts are due to HIV…HIV is cytotoxic to T cells, in vitro at least - in vivo data less convincing”

(ii)                “It's not so much that all individuals with low CD4 counts should get AIDS OIs, or that all people with AIDS-OIs will have a low CD4 count.”


Here Nicholas Bennett himself has demolished the cornerstone of the “HIV” theory of AIDS.


The predictions of the oxidative theory of AIDS

1.        AIDS would remain restricted to the risk groups.

2.        The only sexual act leading to AIDS and a positive antibody test is a very high frequency of receptive anal intercourse in either sex.

3.        Both antibody positive and antibody negative drug users will develop AIDS (with a higher frequency in the former) 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.

4.        In Africa there is neither a new disease, AIDS, nor a new virus, "HIV".

5.        The 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 decreased T4 cell numbers.

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.

7.        AIDS can be prevented and treated with antioxidants.

8.        The phenomena which are said to prove infection with "HIV" are the result of oxidation and not infection with a unique retrovirus, "HIV".


In "Looking back on the oxidative stress theory of AIDS" all these predictions are discussed in detail and ample evidence is presented which indicates that the predictions have been fulfilled.


In our rapid response "More on oxidation - the primary cause for AIDS and "HIV", 1 February, we put to Nicholas Bennett 5 questions, to which he responded in his "Re: More on oxidation - the primary cause for AIDS and "HIV"", 2 February, where he wrote: “In response to their questions:

Q1 Does not make sense, since "oxidized tissues" does not necessarily equate to increased SH levels. However it does appear that cellular redox may be affected, if they want to use the correct terminology. A qualified yes.”


We wonder if Nicholas Bennett has read and understood our simple question: "(a) The tissues of AIDS patients and those at risk are oxidised (have decreased SH levels)?   Yes or no.”    Note that we wrote “DECREASED SH LEVELS” and not “increased SH levels” as Nicholas Bennett wrote.  Surely anyone with even a rudimentary knowledge of SHs, redox and oxidation will realise the intimate relationship between the three.    We find it incredible that these three terms have been used repeatedly in this debate and Nicholas Bennett still appears not to be aware of their definitions and relationships.   Furthermore this doesn’t seem to stop Nicholas Bennett making “authoritative” arguments concerning them.  Neither does he appear to be aware that AIDS patients and those at risk have decreased not increased SH levels.


Nicholas Bennett wrote: “Q2 SH levels only predict survival because...

Q3 SH levels are associated with low CD4 T cell counts, and CD4 T cell counts predict survival. So yes on both counts, but since HIV causes a loss of CD4 T cells due to rapid cycling this doesn't mean HIV doesn't cause AIDS. SH levels alone do not predict much since in the absence of HIV infection.”


We are glad that Nicholas Bennett’s answer is “yes” to both questions.   However, we repeat would Nicholas Bennett please tell us where is the evidence that “HIV causes a loss of CD4 T cells due to rapid cycling”?  Is the loss of CD4 due to "rapid cycling" killing or something else?  (AND PLEASE PROVIDE US WITH WELL DOCUMENTED REFERENCES)


Nicholas Bennet wrote: “Q4 HIV can be detected in culture without any use of oxidants and doesn't require "antioxidants" to be inhibited. Most tellingly, since many seem to consider AZT as an oxidizing agent, it seems ironic that AZT inhibits HIV replication in culture of non-stimulated T cells [3] The answer is no on both parts. Please note this data is over 15 years old - one wonders if the Perth Group chose to ignore it during their extensive literature searches. It was the earliest paper I found in the single PubMed search I undertook to confirm this, so was hardly difficult to discover.”


Would Nicholas Bennett please provide references to support his claim that “HIV can be detected in culture without the use of oxidised cells or oxidants and “antioxidants” do not cause its inhibition”.  From his statement we wonder if Nicholas Bennett thinks that both Montagnier and Gallo are wrong.[6 11] Regarding his reference 3, we wonder if Nicholas Bennett actually read either the paper or our analysis of it in our AZT critique.  If he actually read our AZT paper he would have seen our detailed analysis of this paper.  According to the authors, “AZT inhibits HIV replication” only at cytotoxic levels.  They wrote “our results showed that complete DNA copies of the viral genome were formed in the presence of AZT…Whether virus spread occurs by cell-free virus or by cell-to-cell contact, cultures treated with 25mM AZT eventually produced as much virus as the non-drug-treated infected cultures.”


Nicholas Bennett wrote: “Q5 I have not seen data looking directly at SH levels and viral load, but since SH levels correspond to rapid T cell cycling in response to HIV, one might agree that this could happen. Logically, yes.”


We are amazed at Nicholas Bennett’s response which is totally unscientific and irresponsible without looking at the data.   So we wonder how he can simply “pull” his “logically, yes” out of his hat.   Once again we ask Nicholas Bennett where is the evidence (a) that there is a rapid T cell cycling in “HIV” individuals; (b) the cycling is due to “HIV” and not to SH decrease?


Responding to our question:  "If the answers to questions (a-e) [his Q1-Q5] are yes, does it not mean then that the presently available evidence provides significant support for our non-retroviral theory of AIDS and "HIV"?  Yes or no".  Nicholas Bennett responded: “Since the answers to Q 1 through 5 are not all yes, the Perth Group's conclusion does not follow. In fact, it would not follow anyway since they do not rule out the alternative possibility that HIV is causing the raised SH levels.”


We wonder when Nicholas Bennett will realise that we have never nor anybody else (apart from him) claimed that “HIV is causing the raised SH levels”.   Since the reference he gave to support his “no” answer to Q 4 contradicts his claim, unless he has other references which actually support his claim, then surely it follows that the answer is to Q4 is “yes” rather than “no”.


Given that:

(a)   the predictions of the “HIV” theory of AIDS stated by Nicholas Bennett and others have not been realised (Nicholas Bennett himself has provided no scientific evidence showing these predictions have been realised) and Nicholas Bennett accepts that even today there is no evidence which proves the main tenant of the "HIV" theory of AIDS, that is "HIV" kills the T4 cells in AIDS patients and those at risk;


(b)   the eight predictions of the oxidative theory of AIDS have been realised (Nicholas Bennett himself has admitted to the realisation of at least four of them);


(c)   long after our oxidative theory was put forward and fully aware of it, Montagnier, the “discoverer” of “HIV”, “proposed” that oxidation plays a “key” role in AIDS and “HIV” expression (emphasis Montagnier’s);


then it is surprising that some scientists continue to “beat around the bush” in holding to the “HIV” theory of AIDS rather than pursue the oxidative theory of AIDS whose predictions are supported by scientific evidence.



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

2. Griffith BP. Principles of laboratory isolation and identification of the human immunodeficiency virus (HIV). The Yale Journal of Biology and  Medicine 1987;60:575-87.

3. Owens DK, Holodniy M, Garber AM, Scott J, Sonnad S, Moses L, et al. Polymerase chain reaction for the diagnosis of HIV infection in adults. A meta-analysis with recommendations for clinical practice and study design. Ann Int Med 1996;124:803-15.

4. WHO. 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 1994;10:1327-1343.

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

6. Zagury D, Bernard J, Leonard R, Cheynier R, Feldman M, Sarin PS, et al. Long-Term Cultures of HTLV-III-Infected T Cells: A Model of Cytopathology of T-Cell Depletion in AIDS. Science 1986;231:850-853.

7. Montagnier L. Virus. .New York: WW Norton & Company Inc, 1999.

8. Laurent-Crawford AG, Krust B, Muller S, Rivière Y, Rey-Cuillé M-A, Béhet J-M, et al. The Cytopathic Effect of HIV is Associated with Apoptosis. Virol 1991;185:829-839.

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

10. Montagnier L. Apports de la recherche dans la lutte contra le Sida en Afrique. In: Pietteur M, editor. Le sida en Afrique. Belgique: Collection Resurgence, 2004:224.

11. Klatzmann D, Montagnier L. Approaches to AIDS therapy. Nature 1986;319:10-11.


Competing interests: None declared