HIV genomic variations 5 September 2003
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Christopher J Noble,
postdoctoral fellow
Bern Switzerland

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Re: HIV genomic variations

I am continually surprised by the inability of the so-called dissidents to admit they are wrong.

Eleni Papadopulos-Eleopulos writes 'The reason for our delay in answering Christopher Noble's rapid responses is our difficulty in obtaining his reference (3) which is not available in any Australian library. However, we feel that John Kirkham's rapid response "Comparing HPV and HIV" (30 July 2003) adequately addresses this point.'

I obtained my copy of this article (1) from an Australian library. Please get the article and read it. Do not rely on John Kirkham's interpretation. He directly contradicts the content of the paper.

Eleni Papadopulos-Eleopulos continues '(i) the quote concerning H1N1 influenza A was taken from a review on the evolution of RNA viruses. (ii) The evolution rate of H1N1 may be an exception in comparison with other influenza A viruses. However, its evolution rate is not an exception regarding RNA viruses in general. The reviewers obviously considered H1N1 to be a good example in addition to the other RNA viruses they reviewed and we quoted.'

You are still not addressing my point. You referred to a specific example where an influenza A strain appeared in 1977 that was alomost identical to a 1950 strain. This was clearly an exceptional event if you read the literature, yet you present it as the rule. Nowhere in the review that you cite does it state that this is the norm. (2) Rather it states "Other viruses also demonstrate remarkable stability in some situations". Note the words 'remarkable' and 'some'.

Most importantly nowhere in the review does it state "the genomes of the most variable RNA viruses do not differ by more than 1%"

This is clearly your invention. I ask you to provide evidence to substantiate your claim.

Eleni Papadopulos-Eleopulos continues 'Let us be very clear on this point. We are not considering genomic differences between immunodeficiency viruses of humans, monkeys, cats, etc. We are only interested in the genomic variation in one immunodeficiency virus, the "human immunodeficiency virus". Neither are we interested in the genomic variation with time, that is, evolution of the genome, but the genomic variation at a given time.'

Let me be absolutely clear. You consistently misrepresent the papers that I have provided if you even bother to read them. If you had bothered to actually read the paper on Influenza A that I cited (3) you would have seen in figure 6 that the subtype H3 (A/Texas/1/77) hemagglutinin is as distant from subtypes H1 (A/New Jersey/11/76) as any of the others. I take it you understand what a phylogenetic tree is? Both of these strains are isolated from humans at approximately the same time. If you had bothered to look at table 3 you would have seen that these two subtypes of hemagglutinin from influenza A, isolated from humans at approximately the same time, differ from each other by 81% at the amino acid level.

Why do you continue to dispute these basic facts?

I also challenge you to distinguish the influenza A isolates A/New Jersey/11/76 and A/Texas/1/77 from each other by electron microscopy.

I asked for references showing that nef deleted HIV strains are not attenuated and you reply with a study entitled "Live attenuated, multiply deleted simian immunodeficiency virus causes AIDS in infant and adult macaques".

As you are an expert in genetics and molecular biology that has advised the government of South Africa on these issues I find it hard to believe that these mistakes are due to ignorance. The only conclusion that seems plausible to me is that you are deliberately and intentionally deceiving people.

(1) Halpern AL, J Clin Virol. 19 (2000) 43-56

(2) Steinhauer DA, Holland JJ. Annual Review of Microbiology (1987) 41:409-433.

(3) N. Saitou, M. Nei, Mol. Biol. Evol. 3 (1986) 57.

Competing interests:   None declared