Yet More on Oxidation – the primary cause for AIDS and “HIV” 23 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: Yet More on Oxidation – the primary cause for AIDS and “HIV”

Yet More on Oxidation – the primary cause for AIDS and “HIV”

In his rapid response “Re: More on Oxidation – the primary cause for AIDS and “HIV” (2 February 2005), Nicholas Bennett wrote: “In reply to the Perth Group.

The cause of their "oxidative status" is simply rapidly cycling T cells, in response to chronic HIV infection.”

We repeat, would Nicholas Bennett now agree with us that: (a) individuals belonging to the AIDS risk groups are constantly subjected to semen, factor VIII, recreational drugs, including nitrites; (b) all of them are strong oxidants. If so, how is it possible for them not to affect the cellular redox?

Would Nicholas Bennett please tell us where is the evidence that the T cells are rapidly cycling in response to chronic “HIV” infection and that this cycling is the cause of oxidation? It is a fact that individuals belonging to the AIDS risk groups are exposed to nitrites, factor VIII, recreational drugs and semen and that all of them are strongly oxidising agents. It is also a fact that one of the consequences of malnutrition is oxidation? One wonders why Nicholas Bennett and all the other "HIV" experts ignore this obvious fact to which we have been drawing their attention since the beginning of the AIDS era.

Nicholas Bennett wrote: “I am not aware at all that the very same kit (provided by the same manufacturer) is interpreted differently in different countries. The "same" test may of course be manufactured in different ways by various companies.”

It is pitiful that Nicholas Bennet, a self confessed protagonist of “HIV” antibody testing, is not aware of this elementary and extremely important fact. He should make enquiries of any one of the companies that manufacture “HIV” Western blots antibody test kits. For example, one of the technical managers listed at Genelabs Diagnostics Pty. Ltd. 85 Science Park Drive #04-01, The Cavendish, Singapore Science Park Singapore 118259 Singapore.

Nicholas Bennett wrote: “HIV isolation is not the only way to ensure detection, since culture will only work if an entity is capable of replication.

It is the same reaction in some culture detection methods (others use RT-activity) but the reaction is of course reversed! To most people, being able to detect antibodies from the host AND antigen from cultures from the host is highly indicative of an infection. Most people clearly do not include the Perth Group!”

We repeat, would Nicholas Bennett please tell us how he and “most people” can obtain the “HIV” antigens without "HIV" isolation and determine the specificity of the “HIV” antibody test without comparing the antibody tests with a gold standard which can only be “HIV” isolation?

Note: We repeat that “being able to detect antibodies from the host AND antigen from cultures” are one and the same reaction. And thus “culture” is not synonymous with “HIV” isolation and cannot be used as a gold standard for the antibody tests.

Nicholas Bennett wrote: “Since the sequences detected in viral load are those of HIV, by definition viral load IS good evidence for ongoing viral replication.”

This appears to be his reply to our request: “Would Nicholas Bennett please 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.” We wonder why he did not provide any references? Where is the evidence that “the sequences detected in viral load are those of HIV”? Would Nicholas Bennett please tell us if viral load proves “HIV” infection, why isn’t anybody using it as a test for “HIV” infection? And why does the CDC recommend against this practice? Thus:

In adults, adolescents, and children infected by other than perinatal exposure, plasma viral RNA nucleic acid tests should NOT be used in lieu of licensed HIV screening tests (e.g., repeatedly reactive enzyme immunoassay)” (emphasis in original).[1]

Nicholas Bennett wrote: “The Perth Group themselves have shown that antivirals inhibit HIV replication. In their paper "A Critical Analysis of the Pharmacology of AZT and its Use in AIDS " they cite literature showing reasonably well that the percentage of cells containing HIV-DNA does not change under antiretroviral therapy. However, they don't compare the situation with UNTREATED HIV patients, in which case the percentage of HIV-DNA containing cells increases [1]. Additionally, un-integrated DNA (a true measure of active HIV replication, as opposed to the more static proviral DNA load) decreases significantly while on therapy [2].”

Our paper was about AZT and we provided evidence that AZT does not inhibit “HIV” replication. The title of his reference 1 “Levels of HIV-infected peripheral blood cells remain stable throughout the natural history of HIV-1 infection” which refers to untreated “HIV” patients is self-explanatory. In this paper the text reads “PBMC HIV-1 DNA did not correlate with major indices of disease progression, including time following primary infection, time before reaching a CD4 cell count less than 200x106/l, and time before death. The number of PBMC harbouring HIV-1 provirus was relatively constant throughout the clinical stages of HIV-1 infection”.

In regard to treated patients, they wrote: “the mean HIV-1 DNA level of specimen obtained during antiretroviral therapy was slightly higher than in the absence of antiretroviral drugs.”


Since: (a) by definition all the anti-"HIV" drugs used at present do not inhibit "HIV" replication, they can decrease the "viral load" only by decreasing the number of newly infected cells, that is the "HIV" DNA; (b) there is no decrease in "HIV" DNA with "HIV" treatment[2] it means that the "anti-retroviral" do not have any effect on "HIV" or that either "HIV" DNA, RNA or both are not "HIV" specific.

Discussing their findings the authors of his reference 2 wrote: “Because of the limitations of our dataset (10 patients), additional studies are needed to assess the impact of HAART on the PBMC HIV-1 DNA in larger and more diverse populations…In a previous cross-sectional study, which analysed the integrated and total HIV-1 DNA load in resting CD4 T cells from infected patients receiving HAART, levels of unintegrated HIV-1 DNA 28-fold higher than integrated HIV-1 DNA were found”

Once again Nicholas Bennett fails to provide references supporting his claims and in fact “throws up” references that contradict his claims. The purpose of this debate is to solve a scientific problem, namely, “What is the cause of AIDS?” If he aims to argue for the “HIV” theory of AIDS, then his continuous contribution to this debate with long (sometimes unrelated) yarns and lack of scientific documentation are not helpful.

Nicholas Bennett wrote: “Rather ironically the Perth Group's AZT critique appears to support its use as an antiretroviral.”

This is absurd. Would Nicholas Bennett quote where in our AZT critique have we presented evidence to “ support its use as an antiretroviral”? Has Nicholas Bennett actually read our AZT critique?[3]

In his rapid response to James Whitehead “Re: Re: More on Oxidation – the primary cause for AIDS and “HIV”” (8 February 2005), Nicholas Bennett wrote: “I do not deny that AZT affects the mitochondrial control of the redox state, but I find it ironic that if so it cannot possibly fit with the Perth Group's assertation that HIV is only induced under oxidative conditions, since AZT inhibits HIV replication [1, 2, 3, 4]. Most importantly it does so selectively to cellular toxicity.”

Similarly we wonder if Nicholas Bennett has actually read the references he has provided. The first three were analysed in our AZT paper.[3] Although we have not read the fourth we note that in the abstract there is no mention of the effect of AZT on “HIV” replication. Everybody should know that AZT used in clinical practice is non-phosphorylated and, according to the authors of Nicholas Bennett’s first reference, “the unphosphorylated compound [AZT] does not inhibit reverse transcriptase [“HIV”] per se”. Nicholas Bennett gave an incomplete title for his second reference, the complete title is: “Phosphorylation of 3'-azido-3'-deoxythymidine and selective interaction of the 5'-triphosphate with human immunodeficiency virus reverse transcriptase” [emphasis ours]. There are important differences between the non-phosphorylated and triphosphorylated AZT, including redox. The sentence “Most importantly it does so selectively to cellular toxicity” is another example of Nicholas Bennett’s inane and meaningless yarns.

In the same rapid response to James Whitehead, Nicholas Bennett wrote: "I cannot explain what is meant by oxidative stressors, since this seems to be a phrase most often used by the Perth Group!"

We have never used the phrase "oxidative stressors". Nor do we intend to use it. It is Nicholas Bennett who used it, and we have asked what does he mean by "stressors".

Getting back to his rapid response of 2nd February 2005, Nicholas Bennett 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 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 having 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 prevent 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 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 oxidated cells or oxidants and that “antioxidants” do not cause its inhibition”. From his statement we wonder if Nicholas Bennett thinks that both Montagnier and Gallo are wrong.[4 5] 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) there is a rapid T cell cycling in “HIV” individuals; (b) the cycling is due to “HIV” and not to SH decrease?

Replying to our question "If the answers to questions (a-e) [Nicholas Bennett's Q1-Q5] are yes, does it not mean that the presently available evidence provides significant support for our non-retroviral theory of AIDS and "HIV"? Yes or no". Nicholas Bennett replied: “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 realize that neither we nor anybody else (apart from him) has ever claimed there are raised SH levels in AIDS patients and those at risk or that “HIV is causing the raised SH levels”. Since the reference he gave to support his “no” answer to Q4 contradicts his claim, unless he has other references which actually support his claim then surely it follows that the answer is “yes” rather than “no” to Q4 as well.

Nicholas Bennett wrote: “I'm surprised that the Perth Group state that "scientific thought does not count" when all they have provided to the world of HIV/AIDS research is opinions and scientific thought. One clearly has to add caveats to a dogmatic statement e.g. "HIV replication requires stimulation in some cell lines but not all". The caveat neatly destroys their hypothesis that stimulation is required for HIV expression - perhaps that is why they choose not to use it. Another would be "SH levels correlate with progression to AIDS, but perhaps because they are linked to CD4 T cell count which is itself independently linked to AIDS". The loss of CD4 T cells makes rather more immunological sense than a non-specific affect on global cellular redox.”

Once again Nicholas Bennett takes only a phrase of what we wrote rather than quoting it in its proper context. We wrote “He [Nicholas Bennett] should not debate if he doesn’t have any scientific evidence. Opinions and/or “scientific thought” do not count.” So we repeat that without any supporting scientific evidence his “scientific” thoughts and/or opinions do not count.

We would like to point out to Nicholas Bennett that “stimulation is required for “HIV” expression” is not our hypothesis but an experimental fact. If he chooses to dispute this, would he please give us the references to support his “caveats”. It appears that again Nicholas Bennett has missed the fact there is a better correlation between SH levels and progression to AIDS independent of CD4 T cell counts, than there is a correlation between CD4 T cell counts and progression to AIDS.[6]

Nicholas Bennett wrote: ‘Perhaps the Perth Group can return the favour by responding to the following questions:

Q1 Why should a sexually transmitted disease be expected to be equally bi-directionally transmitted? There is no reason to assume this to be the case, especially considering the animal data [4], the fact that a male inoculum is far larger than a female's, and the fact that homosexual males are a largely sexually distinct risk group.”

We never claimed that sexually transmitted diseases are “equally bi-directionally transmitted”, nor do we expect such transmission. What we have claimed and supported with many references is that there is no evidence, even today, that “HIV” is bi-directionally sexually transmitted. Furthermore, we specifically gave Nicholas Bennett references showing that “HIV serology”, like pregnancy, is sexually acquired but not sexually transmitted. Nicholas Bennett has failed to address this point. For more than 20 years the "HIV"/AIDS experts have claimed 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. Incredibly, the only reference Nicholas Bennett could provide (ref. 4) in support of his claim, is a paper on murine retroviruses.

Nicholas Bennet wrote: “Q2 Why do they say that Montagnier failed to distinguish retroviral RT from mitochondrial DNA polymerase, when his 1983 "isolation" paper clearly states the opposite?”

Montagnier detected RT activity in 3 cultures. The only statement regarding its relationship to “HIV” was “That this new isolate [RT activity] was a retrovirus was further indicated by its density in a sucrose gradient, which was 1.16”. However, by now Nicholas Bennett should be fully aware that Montagnier’s 1.16 band contained no particles which looked like retroviruses. This must mean the RT activity detected in the 1.16 band could not be “HIV”.

Nicholas Bennett wrote: “Q3 Can they show that individuals treated with chemotherapy and "other oxidizing agents" develop a progressive, specific decline in the single subset of CD4 T cells which is reversed by the addition of nucleoside analogue (in the case of HIV, RT inhibitor) medications?”

Individuals exposed to oxidising agents do develop a decline in the subset of CD4 T cells. See HERE. It is difficult to see how the second part of Nicholas Bennett’s question contributes to this debate. If he want to claim that increase in T4 cells, if any, after treatment with RT inhibitors proves that the cause of the decrease in AIDS patients is “HIV”, then he is wrong. We and others (Rapid Responses for Mhlongo and Maduna have presented evidence that the increase in T4 cells by antiretrovirals, if any, may be due to a mechanism unrelated to any “HIV” effects. If the increase in T4 cells in “HIV” infected individuals is due to an effect on HIV replication then how does Nicholas Bennett explain the increase of T4 cells by AZT in non-infected individuals? Which may approach double over pre-treatment levels? See

1. Levy JA, Ramachadran B, Barker E, Guthrie J, Elbeik T. Plasma viral load, CD4+ cell count and HIV-1 production by cells. Science 1996;271:670-671.

2. Milazzo L, Vaira LM, Cremoni L. CD4+ lymphocyte count variations in HIV-negative subjects treated with zidovudine. AIDS 1996;10:1444-5.

How does he know the same mechanism does not operate in “infected” individuals? And what is his proof?

Nicholas Bennett wrote: “Q4 Do they accept the National Cancer Institute's statement that Kaposi's Sarcoma is massively increased in frequency in immunosuppressed people?”

We agree that Kaposi’s Sarcoma is “massively increased in frequency in immunosuppressed people”. But surely Nicholas Bennett is aware that everyone has accepted that the cause of Kaposi’s Sarcoma is not immunosuppression.

Nicholas Bennett wrote: “Q5 Do they accept that a RT activity level in a culture spiked with virus compared to an uninfected culture is therefore due to the presence of the virus as per the method of Potts? [5]”

The answer is yes provided that you put in a virus which has been shown to have RT and you put nothing else which also has RT or can activate cellular RT.

Nicholas Bennett wrote: “Q6 If the anti-HIV antibodies are non-specifically induced and are caused by the same thing that causes AIDS, why does lower anti-HIV antibody levels correlate with worse progression? [6]”

If by this question, he implies that lower anti-“HIV” antibody levels lead to increased “HIV” levels and thus worse progression, then he contradicts himself as seen in one of his responses to Peter Duesberg where he wrote “The thing is, antibodies aren’t the main antiviral response so to use them as the prime rationale for assuming immune control of a virus is wrong…The fact that antibodies may exist and may bind doesn’t mean they will necessarily neutralize nor control infection.” [ Extract Dean’s World 8 February 2005] We agree that antibodies do not neutralize viruses. Responding to Peter Duesberg, Nicholas Bennett also stated that “ …the antibody levels drop just prior to clinical AIDS” and that this “may also be simply an effect of the B cell dysfunction.” [ Extract Dean’s World 8 February 2005]

Nicholas Bennett wrote: “Q7 Why does HIV-specific RNA levels correspond to the rate of CD4 T cell loss? [7]”

We agree with James Whitehead’s response to this (“Re: Re: More on Oxidation – the primary cause for AIDS and “HIV”, 7 February 2005). Montagnier, the “discoverer” of “HIV” does not seem to agree with Nicholas Bennett. At the European Parliament Meeting, 8 December 2004, he showed the following graph:

As can be seen from the 2nd to the 11th year the “HIV” specific RNA levels are approximately constant while the T4 cell number decreases approximately 30-fold from about 800 to 30.[7]

Nicholas Bennett wrote: “Q8 If non-HIV stimuli cause spontaneous antibody, RNA and antigen formation coincident with CD4 T cell decline, what possible genetic mechanism can explain this spontaneous appearance in a subset of host cells?”

We have repeatedLY claimed that oxidation will lead to genetic and PHENOTYPIC changes and have presented scientific evidence to support this claim. See

Nicholas Bennett wrote: “Why not consider an infectious retrovirus?”

An infectious retrovirus has been considered for more than 20 years wasting a lot of people’s time and billions of dollars and still nobody including Nicholas Bennett can give any scientific evidence showing that the "antibody, RNA and antigens" are those of a retrovirus "HIV" or that “HIV” causes a decline in CD4 T cells.


1. CDC. Guidelines for national human immunodeficiency virus case surveillance, including monitoring for human immunodeficiency virus infection and acquired immunodeficiency syndrome. Centers for Disease Control and Prevention. Morb Mortal Wkly Rep 1999;48:1-27, 29-31.

2. Papadopulos-Eleopopulos E, Turner VF, Papadimitriou JM, Alfonso H, Page B, Causer D. Questions about results reported with potent antiretroviral therapy for human immunodeficiency virus type 1 infection. J Infect Dis 2000;181:1518-1519.

3. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D, Alphonso H, Miller T. A critical analysis of the pharmacology of AZT and its use in AIDS. Curr Med Res Opinion 1999;15:1s-45s.

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

5. 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.

6. Herzenberg LA, De Rosa SC, Dubs JG, Roederer M, Anderson MT, Ela SW, et al. Glutathione deficiency is associated with impaired survival in HIV disease. Proc Natl Acad Sci U S A 1997;94:1967-72.

7. 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: pps 224.

Competing interests: None declared