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Nicholas Bennett,
Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY

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According to the Perth Group:

"Not all cell deaths are caused by UV irradiation. However, UV radiation cell death, like apoptosis, is the result of oxidation."

How strange - I was under the impression that the formation of thymidine dimers, C to U transitions and double-stranded DNA breaks (among other mutations) had something to do with things...

The simple fact that HIV "phenomema" are not present in "stimulated" (by the Perth Group's definition) cultures but only in those exposed to the genetic material of HIV or purified virus preps from culture, is sufficient to prove to most people that they are an effect of viral infection. Are they seriously suggesting that the random oxidation of "SH groups" would lead to the spontaneous organistion of over 9,000 bases of DNA into a fully replication competant virus structure?! That is the only explanation that would fit the facts (which are that HIV genomes can be detected in infected but not uninfected cells).

I have already given my definition of proof for the existance of an exogenous retrovirus, by explaining how an infectious molecular clone of HIV was obtained. I cannot be expected to convince a group of people who have shown no inclincation to listen to the facts or accept their errors.

The Perth Group say that "HTLV was isolated from HUT-78". Could the Perth Group please give the citation where HTLV was isolated to the same ludicrously stringent criteria they ahve previously required for HIV isolation? If not, I see no reason why I should believe that HTLV even exists!

As regards KS, several papers and sources have already been referenced showing that HIV massively increases the risk of KS, but that it is not sufficient nor necessary. As such asking for "proof of causation" is a strawman argument: you may as well ask for the paper proving that smoking causes lung cancer. After all, so does asbestos, and not all smokers get lung cancer...

The same has been shown for HHV8 with the exception that HHV8 does seem to be necessary for KS, being present in about 95% of tissue samples.

It is clearly an infectious disease since it is caused by an exogenous virus and transmission of HHV8 has been documented and seroconversion precedes disease. Such studies have also shown that transmission risk is most likely to be sexual in nature, with a particular emphasis on receptive anal intercourse being more efficient than vaginal intercourse.

This data takes all of 20-30 mins to discover in Pubmed: one wonders again why the Perth Group are not doing so for themselves.

Selected Refs:

1. Kedes et al. Nat Med. 1996 Aug;2(8):918-24. The seroepidemiology of human herpesvirus 8 (Kaposi's sarcoma-associated herpesvirus): distribution of infection in KS risk groups and evidence for sexual transmission.

2. Perna et al Int J Epidemiol. 2000 Feb;29(1):175-9. Antibodies to human herpes virus type 8 (HHV8) in general population and in individuals at risk for sexually transmitted diseases in Western Sicily.

3. Diamond et al. 1: Sex Transm Dis. 2001 Mar;28(3):176-83. Seroepidemiology of human herpesvirus 8 among young men who have sex with men.

4. Cannon et al. N Engl J Med. 2001 Mar 1;344(9):637-43. Blood-borne and sexual transmission of human herpesvirus 8 in women with or at risk for human immunodeficiency virus infection.

Competing interests: None declared