Various responses to the Perth Group 9 September 2004
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Nicholas Bennett,
Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY

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Re: Various responses to the Perth Group

Contrary to the Perth Group's 1975-based theory on SH groups, the action of UV light is purely and simply to catalyse covalent modification of the DNA strand. Photons carry a certain amount of electromagnetic energy, as it happens. Eyesight is testimony to is Einstein's work.

Chris Noble has already answered their incredible statement regarding HIV and KS, but introducing them to the concept known in epidemiological circles as "relative risk".

And I was boggled, absolutely stunned, to read at the end of their reiteration of misunderstandings regarding RT that:

"This is the first time that we have read (or heard) that the specificity of the retroviral reverse transcriptase can be determined on the basis of the "RELATIVE amounts"."

This clearly highlights their inexperience in the field of practical scientific research, or more likely, common sense.

It is mind-numbingly obvious: endogenous "RT" activity can be detected in certain cells at certain times, the Perth Group have repeatedly given us references to support this which have not been denied. This "RT" might indeed be the reverse transcriptase component of telomerase, the mitochondrial DNA polymerase, or perhaps other less well- known enzymatic activities. But how does one distinguish it from viral RT? By simply comparing the activity to a baseline in normal, uninfected cells. This is common sense, in the same way that one can demonstrate an increase in lung cancers in smokers above the level seen in non-smokers (so-called "atributable risk"). The trick is called "subtraction" or sometimes "division" to get a relative increase.

I have provided example values from a real experiment here before, but shall do so again.

Blank buffer-only control: 4-6 counts.

Uninfected cells: 20-30 counts.

Infected cultures: 100-2000+ counts (depending on efficiency of infection/transfection and days post-infection)

Positive control: 0.5ul MMLV-RT 10,000+ counts.

Sometimes the uninfected cells give higher background levels, say 50- 100 counts, in which case unless the virus counts are also much higher they have to be discarded. The actual counts are based on variables such as stringency of the SSC washes, age of radioisotope, as well as the amount of RT present: this is why positive and negative samples are run every time.

I typically expressed virus RT as a value relative to uninfected cells, since in a 200-day long experiment it best accounted for changes in radioisotopes, buffers etc. In a typical 14-28 day replication experiment, if all samples are run at once there's no need to do that.

If the Perth Group's original rebuttal of Montagnier's work was based on a mere lack of understanding of relative RT expression (exactly the same as seen in any other enzyme assay) then it's almost laughable, if it weren't so sad. So much angst created from ignorance.

I've already commented on and provided evidence supporting the role of HHV8 in KS in a reply to "HIV HHV8 and KS", and shan't do so again. As far as HPV is concerned, any physician at all knows this. Any virologist knows this. Those in the field are aware that the better the tests are, the more subtypes of HPV are detected, so cervical cancer does seem to be a purely infectious disease. By asking for proof of this fact of viral oncogenesis the Perth Group are, once again, highlighting their ignorance. How they judge themselves competant to pass comment on the field beggars belief.

Competing interests: None declared