Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY
Send response to journal:
It has come to the point where further "debate" with the Perth Group is useless: they will not learn.
They quote irrelevant older science as current. They misunderstand clear statements and misrepresent research findings. All this is well documented: more recently examples include:
If "The cells are FULL of poly(A) RNA", the 1.16g/ml band is full of microvesicles, which contain poly(A)-RNA;  then how is it possible to claim that the poly(A)-RNA in this band is the "HIV" genome?
1. Ayra SK, Gallo RC, Hahn BH, Shaw GM, Popovic M, Salahuddin SZ, et al. Homology of genome of AIDS-associated virus with genomes of human T- cell leukemia viruses. Science 1984;225:927-929.
When a BLAST comparison of HIV and HTLV clearly shows the difference. Full-length HIV genomes obtained from cultures are obviously different from those of HTLV, and the older papers prior to these details are bound to confuse two genetically-similar viruses!
Do they realise that by questioning the "Poly (A)" RNA band they undermine every part of retrovirology prior to HIV? The techniques of sequencing and restriction digests confirm the RNA identity. In the past the Gold Standard of retrovirus RNA detection was by poly A content and density!
They say that HIV cannot kill T cells and quote papers investigating HIV-induced T cell death, and long-term culture techniques. Hardly conclusive evidence. Are they expecting HIV to lyse cells similarly to, say, adenovirus? Regardless of innoculum and cell growth kinetics? Please.
I love the way they quote a 1987 categorisation of retroviruses when the definitions were revised in 1995 and again in 1999/2002/2004! This behaviour is typical sadly, and undermines their entire premise.
The questions they ask are easily answered by a quick browse of the literature or a decent systemic review article. They note that other contributers to this discussion have been reticent in replying of late, and I politely suggest that perhaps they are quite frankly fed up with wasting their time trying to educate the uneducatable. The thought has crossed my mind.
Their AZT critique is particularly amusing, since it neatly proves that it works as an antiviral. Aside from their theoretical argument that AZT cannot work (despite in vitro and in vivo evidence to the contrary) one point made is that under AZT treatment the ratio of infected to uninfected cells remains steady.
What they fail to note is that in UNTREATED infections the ratio of infection to uninfected cells CLIMBS. Therefore, under AZT there is clear control of the virus and benefit. I pointed this out to Todd Miller (an apparent Perth Group contributer) in July 2000  despite the fact that the paper in question was published a year prior to their own critque. Could it be <gasp> selective literature quoting?!
I have read the oxidated stress papers from the Perth Group: they fail utterly to explain the selective loss of CD4 T cells, as I outlined previously. When they say that my statements on GSH are "amazing" I suggest that if they actually presented a cogent arguement supported by properly interpreted literature, a few more "amazing" events might occur.
I would consider it equally "amazing" if the Perth Group were to catch up with the rest of the scientific world and accept things like serology, virus culture and PCR.
As regards the relative RT amounts, my experiments (and those of many other researchers) can be neatly summarised as follows:
Transfect sequence-proven HIV proviral plasmids, or empty plasmid control.
Harvest virus, perform RT assay.
Add equal amounts of RT of each prep to second cell line.
Perform RT assay on a regular basis of second cell line.
A neat control is the use of envelope-deleted proviruses, which produce RT from the initial transfection but do not grow in culture. Only infectious proviral plasmids produce a culture, which can either be acute (cells die after 2-3 weeks) or chronic (cells grow perpetually, along with virus) depending on the conditions.
All cell lines are treated identically.
So, I'm waiting. No stimulation, only media, FCS and antibiotics to keep the bugs away. Standard 5% CO2 and 37C. Why do the uninfected cultures not produce the same RT levels of the infected cultures? Why shouldn't the higher levels of RT in the infected cultures be attributed to virus?
There is 0.05% CO2 in the atmosphere: burning a flame will result in a higher amount of CO2, even though burning is not the only way to produce CO2 and it exists prior to the burning. The Perth Group logic would state that we cannot assume a fire occured, based on a controlled experiment whereby a lit match is dropped into a petrol canister (versus an unlit match) and the CO2 is measured.
Unless the Perth Group publically acknowledge that they have repeatedly misrepresented the literature at least as regards viral variability, viral RT differentiation versus cellular activity, HHV8 and KS and increased risk of opportunistic infection if infected with HIV, then I am inclined to respond solely to the more reasonable contributors to the Rabid Responses (pun intended). Sadly I doubt that, since it would ever so slightly undermine their entire raison d'etre.
I would say that I freely admit my description of HTLV as a lentivirus was on the old clinical criteria of it being "lenti" - slow, as per Alex Russell's use of the word for HIV. But hey, one bit of confusion isn't so bad considering the opposition! :-P
1. Cone et al AIDS vol 12 No 17 1998 "Levels of HIV-infected peripheral blood cells remain stable throughout the natural history of HIV -1 infection"
Competing interests: None declared