Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY
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Dr Fenton is quite right - we are unlikely to change the views of the dissenters/denialists. I can probably count on one hand the number of people who have personally contacted me stating that they now realise their mistakes (or rather that they were duped by the mistakes of others). It was perhaps my original (naive) intention several years ago, and in fact I even hoped that to some extent confronting people like the Perth Group and Duesberg directly would remove or solve the problems, or at least come to some form of mutual understanding.
That has not been the case. The level of stubbornness and self- delusion is astounding.
However what concerns me more than the views of a misguided minority of "scientists" (and I use the word in the loosest possible sense), are the effects on the lay public, who don't have the background to properly sort out what is right from what is wrong. The silent "lurker" on health discussion forums is often the next patient in the consulting room, so providing some kind of balance is I think crucial. Several times I and others have reported how the BMJ Rapid Response forums have been mis- quoted and mis-used as gospel health advice.
Of course the trick is to avoid "feeding the trolls", and judging by the recent emergence of two mammoth posts from the Perth Group it appears I have supplied just enough crumbs!
I could respond in turn by spending my time writing into the wee hours dissecting each and every point in their recent missives, but instead I refer them to the answers I and others have given before, and a current edition of Field's. This has all been said before, it's just that they have (once again) demonstrated their inability to comprehend the written word. There are plenty of references and explanation to satisfy their requirement, if they would only open their eyes and minds.
Personally I don't see the point is wasting the time of the readers and myself by re-posting the same information I've already given (e.g that the proteins encoded by the genome were analysed in the Richieri paper) - a point of view apparently not shared by all. I shall though restate the still unanswered questions I posed back in February, with some additional information.
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 , the fact that a male innoculum is far larger than a female's, and the fact that homosexual males are a largely sexually distinct risk group.
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? Why do they ALSO ignore the fact that in their Rey paper the viral RT doesn't work efficiently with poly-dA oligo dT, which is known to work with cellular enzymes? (Table 2) This is a perfect example of cherry-picking the literature to avoid data that conflicts with their theory.
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?
Q4 Do they accept the National Cancer Institute's statement that Kaposi's Sarcoma is massively increased in frequency in immunosuppressed people?
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 prescence of the virus as per the method of Potts?  In the Rey paper they quote can they not see the "minus virus" entry of 490 counts? Do they not think that the counts due to the virus are therefore complete-endogenous = 3994- 490 = 3504. THIS is what I mean by relative amount. Any count above 490 (in that assay run) MUST BE DUE TO SOMETHING OTHER THAN ENDOGENOUS ACTIVITY. How do they explain how every experiment performed to test for an enveloped viral enzyme _worked_? In their world view, none of these experiments should have been successful (e.g. omitting Triton, centrifugation fractionation etc).
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? 
Q7 Why does HIV-specific RNA levels correspond to the rate of CD4 T cell loss? 
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?
Their point about figure 2 in the Rey paper is amusing if only because it shows that only DNA pol alpha co-purifies in the same fraction as RT, and DNA poly alpha is inhibited by actinomycin D to around 5% activity (not 50%!) by around a fifth of the concentration of drug used in the Rey paper. . The fact that they try to add up enzyme activities in different fractions and try to present them as somehow equivalent only highlights their inability to process scientific method. The fact that a NEW PEAK appears only in the infected cells, a peak which is characterised to be different from the others and functionally equivalent to a viral RT, only goes to demonstrate once again how the Perth Group persist in providing their own rebuttals.
"Using poly Cm dG12-18 as template primer, we indentified the 0.2M KCl peak as the only RT peak."
It is not an addition of existing enzymic activities - it is new.
It is viral.
It is HIV.
Nick Bennett email@example.com
1. Portis et al J Virol. 1987 Apr;61(4):1037-44. "Horizontal transmission of murine retroviruses."
2. Potts 1990 "Mini reverse transcriptase (RT) assay", p103-106 in Aldovini and Walker: Techniques in HIV research.
3. Munoz J Acquir Immune Defic Syndr. 1988;1(4):396-404." Predictors of decline in CD4 lymphocytes in a cohort of homosexual men infected with human immunodeficiency virus."
4. Lyles et al J Infect Dis. 2000 Mar;181(3):872-80. "Natural history of human immunodeficiency virus type 1 viremia after seroconversion and proximal to AIDS in a large cohort of homosexual men. Multicenter AIDS Cohort Study."
5. One good example is shown at http://www.nature.com/nature/journal/v419/n6908/extref/nature01046-s1.pdf
Competing interests: None declared