KS and UV 20 September 2004
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Nicholas Bennett,
Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY

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Re: KS and UV

I have previous supplied information that supports the premise of HHV8 being an oncogenic virus epidemiologically associated with KS. The simplest conclusion (Occam's Razor) being that it is the likely cause. Other factors do not share the same association.

The Perth Group say that I have not done so, but I point them in the direction of the many responses here on the BMJ Rapid Responses, in particular one by myself dated 21st August. If the Perth Group choose to ignore them that is their perogative, but they cannot say I did not answer their request. They have clearly read it because it sparked the discussion regarding the carcinogenic properties of water and semen. It contains references that I'm sure will answer most or all of the questions regarding the oncogenicity of HHV8 and epidemiology of KS (if not them directly, then the references within).

In response to requests of support of the poppers/KS theory they quote themselves! How bizarre.

In reply to their question regarding UV irradiation and covalent modification, I can see that a brief bit of physics may help.

UV irradiation includes 260nm, the wavelength at which maximal absorption occurs for DNA (in fact many "quantitative" techniques for DNA use 260nm densitometry). The energy is sufficient to promote bond breakage and subsequent reformation. The major injury is linkage of adjacent thymidines: this acts as a bump in the road for DNA polymerase and RNA polymerase. There are proteins that can detect or repair these defects, and inherited mutations will lead to UV-related tumour syndromes (e.g. xeroderma pigmentosum). p53 indeed, the granddaddy of tumour- suppressor genes, detects thymidine dimers and initiates excision repair mechanisms (or apoptosis, depending on the level of damage).

SH groups may well be involved in cellular signalling cascades, but that's not quite the same thing as saying that a general oxidative state will result in a specific decline of a SUBSET of ONE CELL LINE, which practically is what the Perth Group are trying to convince us of. Far more likely is a virus that not only infects that particular cell line, but induces lytic cell death, cell cycle arrest and signalling dysfunction, and increases immune activation and apoptosis while preventing replacement.

It all seems so simple, when put like that.

Competing interests: None declared