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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A SUMMARY OF OUR DEBATE WITH NICHOLAS BENNETT
Nicholas Bennett is a self-confessed "Expert" in "HIV" and an ardent protagonist of the "HIV" theory of AIDS. So let us summarise his contribution to this debate regarding the existence of "HIV" and two of its main properties, namely killing of the T4 cells and sexual transmission.
The existence of "HIV"
Nicholas Bennett entered the debate with the following sentence: "Further to previous replies concerning published EMs of [purified] HIV, the best example I have seen personally have been those in the paper: Richieri et al Vaccine, 1998 Jan-Feb;16(2-3)119-29". ("Re: HIV EM Purification", 28 June 2004). When we pointed out to him that the EM does not show purified retroviral particles he still insisted that it showed "wall-to-wall virions" ("One AIDS patient will suffice", 6 July 2004).
Nicholas Bennett claimed that our request for a EM showing HIV particles in the bloodstream is "a straw-man argument". We pointed out that according to Hans Gelderblom, it is possible to see particles in the bloodstream, at least in individuals which have particle concentrations of one million/cm3, and that nobody, not even Hans Gelderblom published such EMs. ("Notes from Hans Gelderblom", 7 July 2004; "Where is the virus", 9 July 2004).
Subsequently Nicholas Bennett claimed that in order to prove the existence of the "HIV" genome and proteins and thus "HIV" it is not necessary to purify the "HIV" particles. "In my mind, I actually have to side with Duesberg on the concept that the purist forms of any virus is the molecular clone, and sequencing of viral RNA or proviral DNA (with subsequent analysis) is a perfect acceptable method of proving [the] existence" of "HIV". However, to date nobody, including Nicholas Bennett and the other participants in this debate, could provide one single reference with evidence for the existence of the "HIV-1 infectious molecular clone".
Several rapid responses are in regard to the "HIV" specificity of the reverse transcriptase activity which Montagnier detected in 1983 ("Re: One AIDS patient will suffice", 6 July; "Re: Where is the virus", 10 July; "Re: Where are the proper controls in HIV" research", 20 July; "Montagnier's reverse transcriptase activity", 23 July; "Re: "HIV", HHV-8 and KS", 21 August; "Nicholas Bennett and Montagnier's RT activity", 8 September; "Re: Nicholas Bennett and Montagnier's RT activity", 9 September; "Various responses to the Perth Group", 9 September; "More on Nicholas Bennett and Montagnier's RT activity, 28 September; "Relative values", 29 September; "Repeat the origin of the CK and RT activity cannot be determined by their "RELATIVE" amounts", 11 October; "Re: Repeat the origin of the CK and RT activity", 11 October; "Long irrelevant yarns are actually hard science", 26 October, 2004).
To begin with, Nicholas Bennett claimed that in his 1983 paper Montagnier proved the specificity for "HIV" of the reverse transcriptase activity as follows: "Montagnier's RT prefers Mg2+ at 5mM and pH 7.8…The keyword is PREFERS. DNA pol gamma will work with Mg2+ at pH 7.4…Montagnier also used further confirmatory methods, such as inhibition with Actinomycin D, which does not affect RT [retroviral RT activity] but does inhibit cellular DNA polymerases and RNA polymerases".
We provided the reference to a study by Montagnier himself in support of our claim. We pointed out to Nicholas Bennett that in 1984 Montagnier himself showed that his RT activity was inhibited by 50% with actinomycin and that "DNA pol gamma [and b] will work" with Mg2+ at 5mM and pH 7.8". Hence, since Actinomycin D “does not affect RT [retroviral RT activity]” the RT activity reported by Montagnier cannot be retroviral. Subsequently, Nicholas Bennett did not even mention if he read Montagnier's reference but claimed that the "HIV" RT activity can be distinguished from the RT activity from other sources by its "RELATIVE" amount, but the "Perth Group seem unable to recognise the principle of RELATIVE amounts". We have pointed out that the origin of an enzymatic activity, especially non-specific activities such as RT and creatine phosphokinase (CK) cannot be determined by their "RELATIVE amounts". Nicholas Bennett again claimed that we are wrong and gave a reference which he claimed shows that the origin of CK can be determined by its "RELATIVE" amount. However, the reference he gave us showed the exact opposite.
In our rapid response, "Repeat, the origin of the CK and RT activity cannot be determined by their "RELATIVE amounts", again we gave a reference where Montagnier showed that non "HIV" infected cells, using the same condition as in 1983 have high levels of RT activity. We wrote: "If we are as wrong and dangerous as Nicholas Bennett claims, then he must write to Medical Hypothesis and refute our latest critique of Montagnier's work".
We repeat: (i) The enzyme reverse transcriptase is not specific to retroviruses or even viruses, a fact accepted by such experts in retrovirology as Varmus and Weiss; (ii) the human genome contains endogenous retroviruses (proviruses) and thus reverse transcriptase genes which, given the right conditions, can be activated; (iii) reverse transcription can be induced not only by the enzyme reverse transcriptase but also by the cellular DNA polymerases.
The ex cathedra statement that beyond a certain level RT activity is caused by the reverse transcriptase enzyme of a particular retrovirus is ludicrous. Is Nicholas Bennett suggesting that regardless of variable and unknown concentrations of "viral" and cellular enzymes and their individual activities according to culture conditions, a certain "level" always means "HIV" RT and nothing else? Even if this were remotely possible what is his proof and what is that "level"? In the Montagnier et al paper HERE, to which we have repeatedly drawn Nicholas Bennett's attention and which he has ignored, the authors presented evidence which shows: (i) contrary to what Nicholas Bennett claims, actinomycin D significantly inhibited (50%) the reverse transcriptase activity which Montagnier claimed to be "HIV" RT; (ii) in figure 2 of the Rey and Montagnier paper, in uninfected cells DNA polymerase alpha, beta and gamma had reverse transcriptase activity of approximately 5, 42 and 17 enzyme units respectively. In "infected" cells the level of "HIV" RT was 57 units and the RT activity of DNA polymerase alpha, beta and gamma were 12, 50 and 14 enzyme units respectively. If one totals the uninfected cell enzyme units it comes to 64 which is greater than the "HIV" activity. At what "level" does Nicholas Bennett suggest the reaction becomes "HIV" specific?
In his reply ("Re: Repeat the origin of the CK and RT activity", 11 October) Nicholas Bennett wrote: "Since the Perth Group have issued the invitation to refute them in formal print, I would be happy to do so. Not least because Montagnier's work contributes only to the molecular biology of HIV and not whether or not HIV causes AIDS, his "contribution" to that question ought to be relatively easy to refute. I found half a dozen glaring errors in the abstract alone. The rest of the paper appears to have been repeated ad nauseum on the Rapid Responses, and therefore the material to refute it is also here. Saves me a lot of time." We are still waiting.
Amazingly, after all this, recently but elsewhere Nicholas Bennett wrote: "I called the Perth Group in public on their lie that Montagnier didn't distinguish viral RT from cellular activity. I'm still waiting for a recognition of the fact 6 months later, despite several reminders to do so. They have not even tried to defend their conclusion, just ignored any comments, even though it underpins most of what they argue about HIV being endogenous cellular phenomenon"! (Dean's World; 1.21.2005 4:05pm).
In his rapid response: "Re: Where are the proper controls in "HIV" research", 20 July, Nicholas Bennett wrote: "As to how I know that the majority of scientists agree that HIV RNA and proteins exist, I have to stop myself laughing loud…The Perth Group clearly failed to comprehend the basis of my arguments for the infectious molecular clone….EM is not necessary, because the molecular evidence is so strong…I provided extensive evidence for the existence of a molecular clone already". In another response, Nicholas Bennett claimed that "there are a plethora of infectious molecular clones of HIV-1 in circulation" (Re: Where is the HIV-1 infectious molecular clone?", 14 July).
We asked, ("More on Nicholas Bennett's "HIV" infectious molecular clone", 28 September 2004): "…would Nicholas Bennett please provide evidence for the existence of an "HIV-1 infectious molecular clone" as defined by Brian Foley (not us). "The clone must produce virus particles that are identical by serology, morphology, protein sequences, RFLP, Southern blotting, etc., to the parental virus, and the particles must also be infectious. If a cloned viral genome does not meet these criteria, it is not an INFECTIOUS molecular clone of the virus, be it HIV-1 or any other virus" (Foley’s emphasis).
Nicholas Bennett has not given us even one reference with evidence which proves the existence of an "HIV-1 infectious molecular clone" even by Brian Foley's definition ("Re: "HIV", HHV-8 and KS", 21 August, 2004; "Re: Cell death and oxidation", 1 September, 2004; "Re: Nicholas Bennett and the "HIV-1 infectious molecular clone", 8 September, 2004; "Give us the "HIV" "structure" please", 11 October).
Nicholas Bennett claimed that: "…the presumed HIV RNA actually encodes the presumed HIV proteins". ("Re: Retrovirologist, retroviruses and purification", 2 July, 2004). He made similar claims in subsequent rapid responses. ("Re: Where is the "HIV-1 infectious molecular clone?", 14 July, 2004).
We asked Nicholas Bennett "where is the evidence that the "presumed HIV RNA" that is the poly-A RNA which in sucrose density gradients bands at the density of 1.16 g/ml (the "HIV" genome) "actually encodes" the "HIV" proteins which band at the same density". ("Where are the proper controls in "HIV" research", 19 July, 2004). Nicholas Bennett gave us a long yarn but not one single reference with evidence that the "HIV" RNA encodes the "HIV" proteins ("Re: Where are the proper controls in "HIV" research?", 20 July, 2004).
From the beginning of the "HIV" era we have claimed there is no evidence that the "HIV" antibody tests prove "HIV" infection. The antibody tests have been extensively discussed in this debate and although we repeatedly asked for references which prove that a positive test means "HIV" infection, to date nobody (including Nicholas Bennett) has given us even one reference. We drew Nicholas Bennett's attention to this fact and provided many references in support of our claim. ("Mechanism by which HIV causes AIDS", 29 September, 2004; "Diagnosing "HIV" infection in neonates", 30 September, 2004). Nicholas Bennett gave us long yarns on the "HIV" antibody tests, but not one single reference where their specificity has been determined. (""HIV" mechanisms revisited", 2 October).
Incredibly, in his rapid response: "Re: Diagnosing "HIV" infection in neonates", 10 October 2004, Nicholas Bennett wrote: "The Perth Group do an admirable job of summarising the reasons why serology is a superior diagnostic tool in ADULTS, but of course we were talking about neonates". This statement is not only misleading but very wrong. How is it possible for us, on the one hand to present well documented evidence that at present there is no evidence that a positive test even in one adult proves "HIV" infection and on the other to "do an admirable job of summarising the reasons why serology is a superior diagnostic tool in ADULTS…."? ("HIV" mechanisms revisited", 2 October).
Regarding the antibody tests in neonates in our rapid response: "Re: Diagnosing "HIV" infection in neonates", 1 October 2004, we wrote: "Nicholas Bennett wrote "Negative infants are followed up until their antibodies disappear, usually at 9 months".
In regard to maternal antibodies disappearing by 9 months would Nicholas Bennett please study the findings of the European Collaborative Study and the Ariel Project, summarised in our monograph "Mother to Child Transmission of HIV and its Prevention with AZT and Nevirapine" - pages 44-45 (Reference 5). In brief the arguments is as follows: The European Collaborative Group Study, is the only study providing a detailed analysis of the post partum loss of infant "HIV" seropositivity. The authors reported approximately 23% of children became seronegative between birth and 9 months. However, 59% became seronegative between 9 and 22 months. Since the latter cannot be due to loss of maternal antibodies, (the maternal antibodies have already been lost by 9 months) the only explanation is that either: (i) the antibody test is non-specific or (ii) the children managed to clear "HIV" infection without treatment. If 23% of children test positive because of maternal antibodies, and in 59% the test is non-specific, how can one be certain that the remaining 18% of children will not also serorevert after 22 months? If the test is non-specific in 59% of children one must also question whether such a test can be "extraordinarily accurate" when applied to the diagnosis of HIV infection of mothers, as well as to fathers and adults in the general population.
Again Nicholas Bennett responded with a long yarn but did not discuss the implication of these data in regard to the specificity of the antibody tests in general, not just in neonates. ("Re: Diagnosing "HIV" infection in neonates", 1 October 2004). Indeed, Nicholas Bennett's question "why the dogmatic hand-up with the magical 9 month value" appears to indicate he does not comprehend the implications of such data.
In our rapid response "The "HIV" antibody tests are not diagnostic", 14 October 2004, once again we drew Nicholas Bennett's attention of the facts about the neonatal antibodies and their implications and gave him a reference by researchers from the CDC where the authors reported "a rapid decay" of maternal "HIV" antibody" with a decline to background levels by 6 months (T½ = 28-30 days)". Nicholas Bennett responded with yet another long yarn ("Re: The "HIV" antibody tests are not diagnostic", 15 October 2004, but without giving even a single reference in which the specificity of the "HIV" antibodies has been proven for neonates or adults.
In our rapid response: "Repeat, the "HIV" antibody tests are not diagnostic", 20 October 2004, we reminded Nicholas Bennett once again that since the mother's antibodies disappear by 9 months, the seroreversion after 9 months means either the children eliminated "HIV" or the antibody tests are not specific. Although in one of his earlier rapid responses ("Neonatal HIV", 28 September 2004) Nicholas Bennett wrote: "Infants are followed up till their [mother's] antibodies disappear, usually at 9 months", in his rapid response "Re: Repeat the "HIV" antibody tests are not diagnostic in infants, but are fine in adults", 20 October 2004, he wrote: "why the dogmatic hand-up with the magical 9 month value". The answer is, because this is what the evidence shows and most importantly because it has profound implications regarding the specificity of the "HIV" antibody test in both infants and adults and thus for "HIV" infection (existence) and the claimed causal role of "HIV" in AIDS.
When at the European Parliament Meeting, "AIDS in Africa : What are the priorities as for medical assistance", 8 December 2003, Montagnier was asked if he isolated "HIV" in 1983, he replied: "Bien sûr on avait un virus [virus-like particles?] qui avait une densité de 1.16 en gradient avec une activité transcriptase inverse, et des protéines spécifiques reconnues par les anticorps du patient". (Web translation service at http://world.altavista.com/tr).
However, at present it is well known that:
(i) At the density of 1.16 even after "Roman" effort, Montagnier could not find any particles with the morphological characteristics of retroviruses, much less of a unique retrovirus "HIV";
In 1983 Montagnier, Barré-Sinoussi and Chermann were aware that reverse transcriptase activity is not specific to retroviruses. In 1984 they themselves showed that the template-primer used in 1983, under exactly the same conditions they used in that year, can be transcribed by the cellular polymerases beta and gamma of non infected cells. We are not the only ones to have questioned the specificity of the RT activity detected by Montagnier. On page 81 in John Crewdson's book “Science Fictions: A Scientific Mystery, a Massive Cover-Up, and the Dark Legacy of Robert Gallo”, one reads: "Gallo was questioning the reality of the reverse transcriptase activity" detected by Montagnier.
(ii) Most importantly, since at the 1.16 band they had RT activity but not retrovirus particles it proves that the detected activity was not retroviral;
(iii) Montagnier reacted the proteins of the 1.16 band with serum from his patient BRU. Of the many proteins present in the 1.16 band, 3 (p25, p45, p80) were found to react with the patient serum. They said that p45 (p41) was actin, made no comment regarding p80,and claimed that p25 (p24) was an "HIV" protein and the antibodies which reacted with it "HIV" antibodies.
However, because the antibody cross-react from an antibody-antigen reaction it is not possible to determine the origin of one reactant even when the origin of the other is known, much less the origin of both.
Yet incredibly Montagnier claimed that the reaction between the p25 (p24) protein in the 1.16 band and antibodies in the patient serum proved that the p24 was "HIV" specific protein despite that fact that no retrovirus particles were present in the 1.16 band and the antibodies which reacted with it were "HIV" antibodies despite the fact that their patient had antibodies directed against a plethora of other antigens. This is academic fantasy.
Given the above indisputable facts, would Nicholas Bennett please tell us in 1983 did Montagnier prove the existence of "HIV"
Yes or no.
If yes, what is his scientific basis?
If no, when was "HIV" discovered and by whom?
"HIV" and the T4 cells
The T4 cell killing by "HIV" and their role in the development of AIDS has been discussed in many rapid responses ("Re: "HIV" and KS", 29 September 2004; "OKT3, OKT4 and all that", 2 September 2004; "CD3, CD4 and all the more modern names". 3 September 2004; "Causes of low CD4 counts in AIDS", 14 September 2004; "Mechanism by which HIV causes AIDS", 29 September 2004; "HIV mechanism revisited", 2 October 2004; ""HIV" and AIDS", 16 October 2004; "Re: "HIV" and AIDS", 18 October 2004; "Re" No scientific evidence - no scientific debate", 17 December 2004. Suffice to point out that in the early part of his debate Nicholas Bennett was adamant that the cause of the decrease in T4 cells in humans (in vivo) was "HIV", and at least in part due to their killing by "HIV". However, in his more recent posting he expressed a different and at times contradictory view.
In his rapid response: "Re: No scientific evidence - no scientific debate", Nicholas Bennett simply stated: "HIV" drops CD4 counts and causes the immune-suppression that allows a commensal organism to cause pneumonia (PCP)", without giving any evidence.
In his rapid response: "Re: "HIV" and AIDS", Nicholas Bennett wrote: "HIV induces a state of chronic, abnormal, immune activation with concomitant cytokine skewing that prevents normal T cell replacement from the thymus. Immune deficiency is a result of cell death due to (in part) HIV killing but probably more so apoptosis due to activation".
(a) "activated CD8+ T-cell count, CRP concentration, and intensity of marijuana use were all associated with increased oxidative damage";
(b) as far back as 1994 Gallo stated: ""Oh, the role of HIV is likely to be in increasing these inflammatory cytokines" But we have learned - this should be of interest to everybody that isn't completely married to HIV - that the inflammatory cytokines are reportedly increased in gay men even without HIV infection. Inflammatory cytokines are usually promoted by immune activation, not by immune suppression. So here was a paradox…So the inflammatory cytokines may be increased by HIV, but I wish I knew what else was increasing them before a gay man was ever infected with HIV…The nitrites [oxidation] could be the primary factor" (Gallo’s emphasis). See http://www.virusmyth.net/aids/data/jlpoppers.htm
That is, the cause of "activation" is oxidation not "HIV" as Nicholas Bennett claims.
In his rapid response: "HIV mechanism revisited", 2 October 2004, Nicholas Bennett wrote: "HIV infection ---> immediate CD4 cell loss through:
Trafficking to Lymph nodes  (activated T cells traffic).
Cell death [15, 16]".
In reference 14, "CCR5+ CD4 T lymphocytes were studied in subjects with primary HIV-1 infection (PHI)". The authors do not claim to have shown that the loss of CD4 cells is due to "Trafficking to Lymph nodes", but that "The only decline of CD4 lymphocytes during PHI resulted from depletion of CCR5¯ CD4 T lymphocytes. After antiretroviral therapy, Ki-67 ¯ CCR5¯ CD4T cell counts rapidly increased in the circulation, which suggests that the initial decrease was due to an alteration in trafficking and/or sequestration" (emphasis ours).
Reference 15 is one of the 4 papers published in Science in 1984 by Gallo's team. There is no evidence that "HIV" causes T4 cells death. It is only stated: "That the viruses we have named HTLV-III belong to the HTLV family is indicated by their…cytopathic effects on T lymphocytes (3)…". Reference 3 is the first paper in the series of 4 published in Science, with Popovic as the principle author. Popovic et al did not present evidence that HTLV-III ("HIV") causes T4 cell death. To the contrary, "Some of the clones permanently grow and continuously produce large amounts of virus after infection…" (emphasis ours). Again, in reference 16 there is no evidence that "HIV" causes death of the T4 cells. Thus Nicholas Bennett once again gave us references which do not contain any evidence to support the claims he makes.
We have repeatedly pointed out that at the beginning of the AIDS era:
1. Gallo and Montagnier were aware that a decrease in the number of T4 cells does not necessarily mean cell death or "Trafficking to Lymph nodes", but SIMPLY A PHENOTYPIC change of T4 cells to other T lymphocyte subsets, such as T8 and can be caused by many agents including PHA.
2. The sum (T4 + T8) remains constant.
3. In 1986 Gallo showed that:
“HIV” + PHA ---> decline in T4 cells
“HIV” ---> no significant effect
PHA ---> decline in T4 cells
4. T4 and T8 have similar functions.
5. In 1991 Montagnier showed that
“HIV” + PHA ---> apoptosis
PHA ---> apoptosis
In other words, for a decrease in T4 cells:
For references see http://www.theperthgroup.com/SCIPAPERS/ept4cells.html
One wonders then why this simple explanation has not been accepted and hundreds if not thousands of papers have been published trying to prove the unprovable. That is, that “HIV” decreases the T4 cells.
In a few of our rapid responses we have drawn attention to the fact that in 1986 Gallo and in 1991 Montagnier showed that HIV does not cause T4 cell death by any means including apoptosis.[4 5]
In one such rapid response we asked "Would Nicholas Bennett please tell us, does the Montagnier and Gallo data show that:
(i) "HIV" does not kill or decrease the T4 cells by any means.
Yes or no.
(ii) since the AIDS patients are exposed to repeated stimulation ("infections with various micro-organisms", "allogenic cells such as semen or blood", drugs (including factor VIII), the cause of the T4 decrease in these patients is the stimulation and not "HIV".
Yes or no.
The only reply we had from Nicholas Bennett was the following: "I note again the obsession with the two initial protagonists in the HIV/AIDS story: researchers who have been one very minor part of the puzzle of HIV". (Re: "HIV" and AIDS", 18 October 2004). Maybe we should draw Nicholas Bennett's attention to the view presently held by one of the "two initial protagonists in the HIV/AIDS story", Luc Montagnier.
In his speech to the European Parliament Meeting, "AIDS in Africa: What are the priorities as for medical assistance", 8 September 2003, Montagnier said: "Enfin un des problèmes majeurs non totalement résolu de la pathogenèse du Sida, reste l'explication de la mort massive des lymphocytes T4. Contrairement à ce que l'on croyait il y a quelques années, cette disparition, qui existe dès la période asymptomatique, n'est pas due à l'infection directe des cellules par la souche virale, qui est alors peu cytopathogène, mais à des mécanismes indirects touchant les cellules CD4+ non infectées; celles-ci ont une propension à mourir d'apoptose,…."
Regarding the cause of the T4 cell death by apoptosis Montagnier said “Un des médiateurs de cette apoptose est l'existence d'un fort stress oxydant caractérisé par une prévalence de molécules oxydantes (radicaux libres) sur les défenses antioxydantes de l'organisme: ainsi le taux de glutathion oxydé est-il très élevé, de même que celui des LDL (Low density lipoproteins) oxydées (figure 5).
Ces anomalies ni disparaissent pas totalement après traitement antirétroviral, suggérant qu'elles méritent d'être corrigées par la prise d'antioxydants appropriés. Des études préliminaires indiquent que ce stress oxydant est plus fort chez les patients africains et existe même chez les individus non infectés, du fait d'une malnutrition".
Montagnier also said: "Concomitamment, commence un déclin du système immunitaire portant principalement mais non exclusivement sur l'immunité cellulaire dépendant des lymphocytes T CD4+, qui aboutit finalement à une phase clinique d'infections opportunistes et de cancers qui entraînent la mort".
In summary, according to Montagnier:
(i) the cause of the clinical syndrome and thus death of the patients is T4 cell death;
(ii) T4 cell death is due to apoptosis;
(iii) The cause of apoptosis is oxidation.
In other words the cause of AIDS is OXIDATION.
If the principal cause of the syndrome is T4 deaths and T4 deaths is due to apoptosis which is caused by oxidation, would Nicholas Bennett please tell us what is the role of "HIV" in AIDS?
We would be grateful if Nicholas Bennett would please tell us how Montagnier's present day view concerning the role of oxidation in AIDS can be reconciled with Montagnier’s present day view that "HIV" causes AIDS? (Note that: (i) Neither Montagnier nor anybody else has provided scientific evidence that "HIV" causes oxidation; (ii) In 1992 was Montagnier made aware of our oxidative theory of AIDS (including the causes of oxidation in each risk group) proposed at the beginning of the AIDS era but has never acknowledged it).
If Nicholas Bennett is to be consistent he should now call Montagnier's comments on AIDS and oxidative stress as yet more "drivel" and "holes in the head". And as an HIV/AIDS expert scientist he should make it his immediate business to personally acquaint Montagnier with his views.
In his rapid response "HIV mechanism revisited", Nicholas Bennett wrote: "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 T4 cells, in vitro at least - in vivo data less convincing…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 low CD4 counts".
With this, Nicholas Bennett himself has demolished the cornerstone of the "HIV" theory of AIDS.
Sexual transmission of "HIV"
In his rapid response, "Re: Oxidation - the primary cause for AIDS and "HIV"", 22 January 2005, Nicholas Bennett wrote: "HIV" serology should, obviously, appear to be transmissible and associated with the individuals and risk groups associated with AIDS".
In our rapid response, "More on oxidation - the primary cause for AIDS and "HIV"", 1 February 2005, we have cited several references in which the epidemiological evidence shows that unlike the other sexually transmitted disease which are bi-directional, "HIV" serology", like pregnancy is sexually acquired but is not sexually transmitted.
Incredibly, in his rapid response, "Re: More on oxidation - the primary cause for AIDS and HIV"", 2 February 2005, Nicholas Bennett does not make any comments in regard to the epidemiological evidence we gave him on the unidirectionally acquisition of "HIV serology", and gives a reference for the un-equal transmission of mice retroviruses. Is this the best he can do?
In conclusion Nicholas Bennett entered the debate apparently with the following beliefs:
(a) There is evidence for the existence of “HIV”, namely,
(i) There is EM evidence for the purification of the “HIV” particles;
(ii) The specificity of RT for “HIV” has been proven;
(iii) The existence of the “HIV” infectious molecular clone has been proven;
(iv) The “HIV” RNA codes for the “HIV proteins;
(v) The specificity of the “HIV” antibodies has been proven
(b) The “HIV” decreases the T4 cells by trafficking to lymph nodes and by killing them and in its turn leads to the clinical syndrome.
(c) The “HIV serology”, that is, “HIV” is transmissible by sexual intercourse.
During the course of this debate, Nicholas Bennett was asked to give references to substantiate his beliefs. The references that Nicholas Bennett gave us contained no evidence to support his beliefs and in many cases went against his beliefs. Clearly it is about time that Nicholas Bennett either comes up with the scientific evidence and not yarns (as he chronically has in the past) or starts to question his own beliefs (which even the best scientists do from time to time).
1. Rey MA, Spire B, Dormont D, Barre-Sinoussi F, Montagnier L, Chermann JC. Characterization of the RNA dependent DNA polymerase of a new human T-lymphotropic retrovirus (lymphadenopathy associated virus). Biochem Biophys Res Commun 1984;121:126-33.
2. Crewdson J. Science Fictions. 1st ed. Boston: Little Brown and Company, 2003. pps 670.
3. Stephensen CB, Marquis GS, Douglas SD, Wilson CM. Immune activation and oxidative damage in HIV-positive and HIV-negative adolescents. Journal of the Acquired Immune Deficiency Syndrome 2005;38:180-90.
4. 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.
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. Papadopulos-Eleopulos E. Reappraisal of AIDS: Is the oxidation caused by the risk factors the primary cause? Med Hypotheses 1988;25:151-162. http://www.theperthgroup.com/SCIPAPERS/reappraisalofaids.html
Competing interests: None declared