Re: Genomic Variability 1 November 2003
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Brian T Foley,
HIV Researcher
Los Alamos National Lab, Los Alamos, NM 87545

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Re: Re: Genomic Variability

In an October 14, 2003 Rapid Response, the Perth group wrote:

quote "...
It's true that viruses can vary much more than cells -- human, animal, plant or bacterial cells alike -- because cells are actually the responsible species that have to maintain a reasonable economy in everything to keep things going. A virus is only a parasite. All it needs to do is to take care of its own replication. So a virus has more flexibility to mutate than does a cell. It has to maintain a much smaller budget and a much smaller economy. But the rules in general are still the same. You can mutate certain things, and when you go beyond that, then it's over. It doesn't exist anymore. And, in that regard, HIV is exactly -- and I'm pointing out exactly -- the same as all other viruses. You'll find the same thing with flu and with polio and with measles and with mumps and with other retroviruses in chickens and in mice.

There is nothing special about HIV in that regard. Nothing." (6)

..." end quote

Indeed all sequences of all lentiviruses show that they are constrained to maintain many sites absolutely invariant throughout their evolution. I have already shown this in earlier postings here, for example in my Sept 9th, 2003 posting where I discussed the Asp-175 and Asp-186 in the catalytic core of the reverse transcriptase enzyme.

It is the study of the pattern of evolution of the lentiviruses over time, that gives us the most information about where these viruses came from. The pattern is consistent both within very closely related strains, such as those from a set of sexual partners who have become infected from one another via heterosexual contact (1,2) and across very diverse strains of lentiviruses such as feline immunodeficiency viruses from hosecats, American pumas and African lions (3,4). The Perth group apparently wishes to confuse people by claiming that HIV-1 sequences are unusual in their pattern of evolution, but this is not true; they are typical retroviruses which evolve over time.

1) Leitner T, Kumar S, Albert J.
Tempo and mode of nucleotide substitutions in gag and env gene
fragments in human immunodeficiency virus type 1 populations
with a known transmission history.
J Virol. 1997 Jun;71(6):4761-70.
PMID: 9151870

2) Robbins KE, Weidle PJ, Brown TM, Saekhou AM, Coles B, Holmberg SD,
Folks TM, Kalish ML.
Molecular analysis in support of an investigation of a cluster of
HIV-1-infected women.
AIDS Res Hum Retroviruses. 2002 Oct 10;18(15):1157-61.
PMID: 12402955

3) Olmsted RA, Langley R, Roelke ME, Goeken RM, Adger-Johnson D,
Goff JP, Albert JP, Packer C, Laurenson MK, Caro TM, et al.
Worldwide prevalence of lentivirus infection in wild feline
species: epidemiologic and phylogenetic aspects.
J Virol. 1992 Oct;66(10):6008-18.
PMID: 1382145

4) Brown EW, Yuhki N, Packer C, O'Brien SJ.
A lion lentivirus related to feline immunodeficiency virus:
epidemiologic and phylogenetic aspects.
J Virol. 1994 Sep;68(9):5953-68.
PMID: 8057472

Competing interests: None declared