Department of Medical Physics, Royal Perth Hospital, Western Australia, 6001,
Valendar F Turner, John Papadimitriou, Barry Page, David Causer, Helman Alfonso, Sam Mhlongo, Todd Miller, Christian Fiala
Send response to journal:
Repeat, give us the "HIV" "structure", please
In his rapid response: "Re: Repeat, the origin of the CK and RT activity", 11 October, Nicholas Bennett wrote: "As regards the cellular poly(A) versus viral poly(A), I feel the urge to point out that "Poly(A)" RNA has very very very little, at all, whatsoever, to do with retroviruses."
If the "Poly(A)" RNA "has very very very little, at all, whatsoever, to do with retroviruses", then why has the poly(A)-RNA which in sucrose density gradients bands at 1.16g/ml? been defined as being the "HIV" genome?
Nicholas Bennett wrote: "The cells are FULL of poly(A) RNA. Even in a full-blown retroviral infection merely 1% of the cells poly(A) RNA will be retroviral, the rest will be the host mRNAs. For the non-virologists, 1% cellular RNA being of a viral origin is very high indeed."
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?
Nicholas Bennett wrote: "As regards the formation of a viral structure, I refer the Perth Group to the oft-quoted paper from Richieri et al which I emailed them on the 23rd July. There are of course plenty of other papers out there looking at membrane constituents, full-length genome cloning and protein content – some of which have been quoted here before. I suggest they perform the PubMed search themselves."
In his rapid response: "Re: Five questions to Nicholas Bennett", 23 September, Nicholas Bennett wrote: "One of the intellectual attractions of retroviruses, to me, was that they [their RNAs or cDNA] were able to do all of this and produce an RNA/lipid/protein structure that could do it all again. And all with only 9 genes….".
We have done many literature searches, but could not find even one study with evidence showing that the introduction of the "HIV" RNA (cDNA) into cells, leads to the appearance of "structures", that is particles with the morphology of retroviruses which have the same RNA as that which was introduced in the cells and proteins which are coded by it.
Such evidence, certainly cannot be found in the Richieri paper. In fact in that paper even the first step is not satisfied, that is, Richieri et al did not "infect" their cells by the introduction of the "HIV" RNA (cDNA).
So, for the third time, we repeat our request to Nicholas Bennett.
Would Nicholas Bennett please give us one major study and a few confirmatory studies showing that the introduction of the "HIV" RNA into a cell leads to the production of "an RNA/lipid/protein structure" (?viral particle). That is, would Nicholas Bennett please provide evidence for the existence of an "HIV-1 infectious molecular clone" as defined by Brian Foley (not by us): "The clone must produce virus particles that are identical by serology, morphology, protein sequences, RFLP, Southern blotting, etc., to the parental virus, and the particles must also be infectious. If a cloned viral genome does not meet these criteria, it is not an INFECTIOUS molecular clone of the virus, be it HIV-1 or any other virus" (Brian Foley's emphasis).
(It would be very much appreciated if Nicholas Bennett responds with concrete relevant data and not with long yarns and lectures in biology).
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.
2. Bess JW, Gorelick RJ, Bosche WJ, Henderson LE, Arthur LO. Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations. Virol 1997;230:134-144.
3. Richieri SP, Bartholomew R, Aloia RC, Savary J, Gore R, Holt J, et al. Characterization of highly purified, inactivated HIV-1 particles isolated by anion exchange chromatography. Vaccine 1998;16:119-29.
Competing interests: None declared