Re: Reply to Russell's points 4 April 2005
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Nicholas Bennett,
Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY

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Re: Re: Reply to Russell's points

A single Pubmed search gives the lie to several of Alex Russell's points.

1: He says that HHV8 is ubiquitous. If it were, then one would expect serology to show widespread infection.

2: He says that there are no heterosexual AIDS-KS cases. If that were true we would expect to see no women with AIDS-KS.

Atkinson et al find that: "KS incidence was highest for MSM (5.7 per 100 person-years), substantially lower for heterosexual men (0.7 per 100 person-years), and lowest for women (0.4 per 100 person-years)." [1]

If he chose to question the dissident dogma he might find the very evidence he is asking for. Clearly women and heterosexual men do get AIDS -KS. It is biased towards homosexual men, but not restricted! This data also shows that not everyone has HHV8 infection. His theory of a commensal that reactivates in a certain tissue type is not entirely far- fetched, but since introduction of viral genes can cause the same kind of lesions in animal models (as laid out previously), and serology precedes the disease, clearly the most likely explanation is that the infection comes first.

In addition, his comment that "all STDs have their origin in the heterosexual community and find their way into the homosexual community horizontally through sexual transmission by bisexual men" clearly shows he is forgetting that the introduction of HIV into the west was through homosexuals. They were the first risk group to be identified and several contact tracings show that "patient zero" for a slew of early cases was a gay flight attendant, and similar cases were seen in the "patient zeros" of other chains/networks of infected people in Europe (homosexual, travel to the US or Africa). No doubt if the initial infected person was a heterosexual we would have had a different epidemic profile. It's a simple as that. In areas where HIV was introduced by, for example, IV drug users they are the predominant carriers of HIV.

As regards HIV viability in syringes, this very work has, once again, been performed. Viable HIV has been cultured from syringes after up to 6 weeks at room temperature, albeit at low levels at the later timepoints. [2]

Healthcare workers have been documented to have acquired HIV through occupational exposure via many "anecdotal" cases. As of 2004 the CDC lists 57 definites in the US and a further 139 possibles (other risk factors may explain the infection). [3] 26 have developed AIDS. 5 cases are known from the UK with a further 14 possibles. This a very popular dissident lie that is entirely unsupported - all of these cases are published in the literature, the references are in tables 3 and 4 of the second link.

Duesberg's "HIV-free AIDS cases" are an empty set of clearly non-AIDS patients. Harris points out (as I have been trying to do) that since AIDS is a decline in a specific subset of immune system cells, proper analysis of these "HIV free AIDS cases" shows that they do not have AIDS. By expecting only AIDS patients to have AIDS-indicator diseases both Duesberg and followers like Russell are demonstrating a lack of clinical experience, or simple literature analysis. [4] This over-simplistic black -and-white thinking is characteristic of AIDS denialists, but unfortunately a side effect of media portrayal of science in precisely this manner. By cutting it up into bitesize chunks, one necessarily removes the underlying logic and explanations behind the conclusions.

One form of "non-HIV AIDS", idiopathic CD4 lymphopenia, (ICL) is very different from AIDS - to quote from Harris [4]:

" Moreover, people with ICL were not only epidemiologically, but often immunologically distinguishable from AIDS cases: their CD4+ lymphocyte counts swung widely, and transiently, in response to infections, and were often much higher than 300 (in contrast to people with AIDS, whose CD4+ lymphocyte counts tend to stay low and heading on an ever-downward trend). ICL people also often had low total lymphocytes or low CD8+ lymphocyte counts, again indicating that their immune failure did not make much distinction between CD4+ and CD8+ lymphocytes, as classic AIDS does. Clearly, these people did not belong to the classic AIDS groups which began suffering with epidemic immune problems about 1980. They are not part of the new phenomenon of AIDS, and although sometimes suffering from opportunistic infections, did not even seem to share the implacable death rate of AIDS. {ref 5 below}"

As regards MVV, there is evidence of transmission mainly via infected cells in respiratory secretions. Since one of the primary diseases caused by MVV is a pneumonia this perhaps isn't too surprising. I'm amused that Mr Russell finds it easy to accept literature that supports his view without question, and just as easily dismiss others that do not support it. In contrast, the explanations offered by myself and others fit with the vast majority of the experimental and observational results.

The reader should note that the Padian study did not formally test or control for the use of condoms by the participants, unlike the de Vincenci study. None of the regular condom-users got HIV in that study.

The Perth Group comments, parrotted by Alex Russell, merely highlight a lack of awareness of cloning techniques and simple virology. Viruses vary, especially RNA viruses since RNA polymerases lack proof-reading capability. Influenza is arguably the king of variability and perhaps surpasses HIV with its ability to swap whole genes from one virus species to another. No-one with any experience in the field would actually expect identical length sequences nor identical sequence despositions in Genbank. What is true is that the sequences are on the whole clearly the same virus, as any BLAST comparison will reveal. It's also interesting that they ask for a sequence lengthof 9150, when the accepted HIV-1 sequence length is over 9700 bases (9719 for the reference genome k03455). I worked with a clone of the reference genome that contained 3 mutations, but due to the genetic code none of them affected the actual proteins produced by the genes. The genome does not vary randomly - those areas crucially important in replication remain stable, as one would expect. Most of the variation in natural isolates is in areas used to avoid immune responses or drug effects.

Incidentally, since the sequences do vary, by up to 60% in some regions of the genome, this is actually an argument _against_ Alex Russell's proposition of it being a HERV. As well as postulating an as- yet undiscovered gene sequence (remembering that the human genome has, in fact, been sequenced) and/or a bizarre set of recombination events, he has to explain why diverse sequences from different chromosomal locations should all be able to do the same thing.

I on the other hand, merely have to point to the error-prone enzymes of Reverse Transcriptase and RNA pol II, and cry j'accuse!

Nick Bennett

1. Atkinson et al J Acquir Immune Defic Syndr. 2004 Oct 1;37(2):1282- 1287."The Incidence of Kaposi Sarcoma Among Injection Drug Users With AIDS in the United States."


3. and


5. Int Conf AIDS. 1993 Jun 6-11;9(1): 47 (abstract WS-B06; Int ConfAIDS. 1993 Jun 6-11;9(1):41(abstract WS-A25-5; Int Conf AIDS. 1993 Jun 6-11;9(1): 200(abstract PO-A19-0396); Int ConfAIDS. 1993 Jun 6- 11;9(1):47 (abstract WS-B04-1).

Competing interests: None declared