Re: Yet More on Oxidation – the primary cause for AIDS and “HIV” 23 March 2005
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Nicholas Bennett,
Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY

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Re: Re: Yet More on Oxidation – the primary cause for AIDS and “HIV”

In reply to just two of the more obvious points in the latest Perth Group post:

"Absurd" was the word I also used when reading their AZT critique. The paper I cited does say that the amount of HIV proviral DNA doesn't change during untreated infection, in the same way as the Perth Group refer to papers showing that the proviral load doesn't change much during treated infection. However in treated HIV infection CD4 counts remain steady, whereas they DECLINE year on year if left untreated (a state of affairs not seen in any other immune deficiency disease). As such the overall _percentage_ of infected cells INCREASES. One wonders why the Perth Group would expect RT inhibitors such as AZT to affect pre-existing integrated proviral DNA (which is not subject to or dependant on reverse- transcription).

They also choose to corrupt the study I quoted (one of many available in the literature) that showed that AZT inhibits HIV in vitro by quoting the section that refers to acquisition of AZT resistance (the virus was re -cultured and showed wild-uninhibited replication kinetics in the presense of AZT) [1]. This the classic behaviour of acquired resistance to a drug, not evidence that it doesn't work! If they had performed any kind of laboratory work they would know this. I note that also these cells were unstimulated, contrary to what the Perth Group claim is required to express HIV. Certain cell lines do require stimulation, in the same way as certain cell lines can exist without serum and others can't. The stimulation has been shown to directly affect the proviral promotor, which is a rather better explanation that some unexplained activation of invisible endogenous sequences that cannot be found by Southern blotting.

I urge the reader to go to the website provided below and see if figure 2 is convincing enough in the effects of AZT of RT activity (please note the uninfected control, and the fact that the cells were grown only in RPMI 1640 media with 10% serum - no stimulation).

In addition can they please explain to a simple molecular biologist how factor VIII is oxidative when given as a hemophilia therapy but is not when present as a normal human protein expressed at tens of times higher concentrations. For the unintiated reader the standard active concentration of factor VIII used in replacement therapy is 1-3% of normal levels, which is perfectly functional. Maximal therapy, used for surgery, is 50-100% replacement.

It, along with much of their theories, makes no biological sense. If they didn't obfuscate so much it would be more apparent. I hope that by "cherry picking" these particularly obvious errors I can show the reader that all is not quite as the Perth Group would have them believe.

Nick Bennett njb35@cantab.net

1. Smith et al J Virol. 1987 Dec;61(12):3769-73. "Resumption of virus production after human immunodeficiency virus infection of T lymphocytes in the presence of azidothymidine." http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=255991&blobtype=pdf

Competing interests: None declared