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
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Did Montagnier discover HIV in 1983?
Lately Brian Foley and Christopher Noble have posted a series of responses:
“The methods used to clone HIV are the same ones used to clone other retroviruses”, 5 June 2004; “One simple question for the Perth Group – 2”, 7 June 2004; “Re: New and repeated questions and requests to Brian Foley”, 8 June 2004; “Absence of evidence is not evidence of absence”, 8 June 2004. Since Brian Foley responded to our two questions to Christopher Noble and since the same arguments were used in all these postings we respond to both of them.
Brian Foley wrote:
“The Perth group wrote:
Dr. Montagnier’s group of researchers used the EXACT same techniques to produce their first molecular clone of HIV-1 M group subtype B virus… They cloned the proviral DNA from infected cells to create the Lambda-J19 and Lambda-J81 clones.”
Our questions (Q1 and Q2) to Christopher Noble were clearly linked together and referred to Montagnier’s 1983 paper. Brian Foley’s response is a good example of how in this debate he sidesteps the relevant questions, calls us liars, muddys the waters and gives a totally unrelated response. According to Robin Weiss, “The origin of human immunodeficiency virus type 1 (HIV-1), the retrovirus that is the main cause of AIDS, has been a puzzle ever since it was discovered by Barre-Sinoussi and her colleagues in 1983” (1). In a recent paper Luc Montagnier and Robert Gallo stated that “ a clear-cut isolate” was obtained by Luc Montagnier and his colleagues in early 1983. They also agreed that in his May 1984 Science papers Gallo showed that the virus Montagnier discovered was the cause of AIDS (2). In Montagnier’s 1983 paper and in Gallo’s May 1984 papers no mention is made of an “HIV” genome, “molecular clone of HIV-1”, or that they “cloned the proviral DNA from infected cells to create the Lambda-J19 and Lambda-J81 clones” or any other clone.
Brian Foley wrote: “All of these researchers made use of sucrose gradients for separating virions from the majority of cellular material.”
We are pleased Brian Foley agrees that Montagnier used the method of banding in density gradients to separate “virions from the majority of cellular material”. The problem is that with this method, instead of separating “virions from the majority of cellular material”, Montagnier obtained a “purified virus” which consisted of cellular material that had no particles with the morphology of retroviruses. In his role as "HIV geneticist" at the Los Alamos “HIV” database, does Brian Foley ever wonder how all the nucleic acid sequences he fastidiously catalogues and studies were actually obtained?
Brian Foley wrote:
“The Perth group wrote:
The evidence presented in the 1983 paper with Francois Barre-Sinoussi as the lead author include:
1) The viral RT
activity from HIV-infected PBMCs banded at 1.16 g/ml in sucrose density
Let us consider each of the 6 points that Brian Foley has listed. Points 1, 2 and 5 refer to RT activity. So does point 4 because the only proof they had for passing the “virus” to cultures of “PBMCs from adults and on cord blood lymphocytes from newborns” was the detection of RT activity.
In their 1973 Spectra paper, Barre-Sinoussi and Chermann wrote: “This enzymatic activity can be explained by the presence of some virus particles in these regions, and since similar polymerase activity has been found in normal cells, may be mainly ascribed to the cellular enzyme”. That is, RT activity in banded material may occur in the absence of retroviruses. Since, in the 1.16g/ml band, Montagnier did not have any particles with the morphology of retroviruses, the RT activity in this band obviously was not due to the presence of “HIV” but a cellular enzyme. Nowadays the non-specificity of RT is known even in the popular press to readers contemplating purchase of shares in biotechnology companies (3).
In his 1983 paper, Montagnier did state that the RT activity “was not inhibited by actinomycin D”. However, in 1984 he wrote that the RT activity was reduced “by approximately 50%” without indicating in either of the studies what dose of the drug was used.
It is most interesting that Brian Foley has omitted (either purposely or for some other reason) what Montagnier considered to be one of the most distinguishing features between viral RT and “endogenous cellular activity”. This was the “preferential specificity” of RT for the template primer An.dT. This is another example of where Montagnier ignored previous scientific findings. In 1977 Gallo pointed out that “Like reverse transcriptase, DNA polymerase gamma [a cellular enzyme] prefers” the template primer An.dT “with either Mg2+ or Mn2+ present” (2). Brian Foley’s statement, the "lower pH optimum" for the HTLV-I RT activity compared to that of "The viral RT ["HIV"] activity" is irrelevant. If one wishes to distinguish between the RT activity of “HIV-1” and the “endogenous cellular activity” on the basis of pH, the comparison should be done between the two enzymes, not between HTLV-I and “HIV-1” RT activity. The latter is relevant only if one wants to differentiate between the RT of HTLV-I and “HIV-1” which cannot be done unless the existence of HIV-1 is proven beforehand. In 1978 Gallo pointed out that “Polymerase gamma has a pH optimum between 7 and 8…” (3). In his 1983 paper Montagnier stated "The reverse transcriptase activity [of HIV] had "an optimal pH value of 7.8", which is well within the pH range of the “endogenous cellular activity”. In 1984 Montagnier used the same template-primer as in the 1983 study and reported RT activity with the cellular DNA polymerases (4). Hence it is a mystery why, in their 1983 paper, they stated “PBMCs cultured in the same way, without added virus, were consistently negative for reverse transcriptase activity”.
Summarising, even people who need to be “spoon-fed” can see that RT activity in no way can be used even as supporting evidence to claim the detection of a retrovirus. Much less for the isolation and “passing” of a retrovirus.
Regarding point 3, budding is non-specific to retroviruses. Similar buddings to those observed by Montagnier can be found in non-infected cells (5). In his 1983 paper Montagnier wrote: “That this new isolate was a retrovirus was further indicated by its density in a sucrose gradient, which was 1.16…”. This means that if the buds and the resulting cell-free particles were retroviral then these cell-free particles should have banded at 1.16g/ml. We now know that despite his 1983 claim Montagnier saw no particles in the 1.16g/ml band with the morphology of retroviruses. Therefore it follows that the observed buds were not retroviral. The cell-free particles observed in the culture were reported by Montagnier as being “a typical type-C RNA tumor virus…”. Brian Foley has been “spoon-feeding us” (or so he thinks) that “HIV” is a lentivirus. Perhaps he needs to be reminded that type-C viruses belong to the oncovirus sub-family of retroviruses.
In point 6 the “HIV” is compared with HTLV-I. To do such comparison first one needs to have proof for the existence of “HIV” and the “HIV” p25 (p24) protein. In other words, point 6 cannot be used as evidence for the existence of “HIV”.
In summary, the evidence which Montagnier presented for the existence of “HIV” was RT activity and retrovirus-like particles, phenomena which can be found in non-“HIV” infected cultures especially under the conditions used by Montagnier et al.
Brian Foley wrote: “It is not very important whether or not the evidence in that single 1983 paper is enough to convince Christopher Noble that HIV exists. There have been several thousand other papers published before and after this paper which reconfirm the evidence that HIV-1 M group viruses are the cause of the majority of AIDS cases in humans, and that the HIV-1 N and O groups and several groups of HIV-2 viruses contribute very little to the pandemic.”
Once again, Brian Foley pretends to answer the question put to Christopher Noble which refers directly to Montagnier’s 1983 paper. Again he sidesteps the question which was on the existence of “HIV” and talks about the “cause” “of AIDS”. Brian Foley states there “have been several thousand other papers…which reconfirm the evidence…”. How does Brian Foley know this as a fact? Has he read and analysed them all? When we have previously asked for such references Brian Foley responded with a list which contained no such evidence. If Brian Foley has indeed read and analysed these references we would be grateful if he would provide the evidence which led him to conclude that “HIV” exists.
Let us paraphrase our question Q2 to Christopher Noble:
Does the evidence in the Montagnier 1983 study convince Brian Foley and Christopher Noble that “HIV” was discovered.
Yes or No?
Brian Foley wrote: “For the past several years, the Perth group has been implying that Francois Barre-Sinoussi and Claude Chermann had created some “rules” for virus isolation in 1973. Because the Spectra paper (1) contained no such rules, I was under the impression that the Perth group was referring to some other paper or talk that I had not seen.”
We are referring to another paper. We are astounded that Brian Foley is not aware of this paper because we have repeatedly referred to it in this debate. This paper is by Toplin (8) and was published in the same issue of Spectra as the Barre-Sinoussi paper. At present it can be accessed on our web site (http://www.theperthgroup.com/OTHER/Toplin.pdf).
Brian Foley wrote: “In fact, the Spectra paper describes sucrose gradient separation of viral particles from the majority of cellular contaminants, but does not lay down any rules at all for “virus isolation”.
We are glad that Brian Foley agrees that the Barre-Sinoussi Spectra paper “describes sucrose gradient separation of viral particles from the majority of cellular contaminants”.
1. Weiss RA, Wrangham RW. From Pan to pandemic. Nature 1999;397:385-386.
2. Gallo RC, Montagnier L. The discovery of HIV as the cause of AIDS. N Engl J Med 2003;349:2283-5.
3. Pachacz M, 2001. No need to be phased. Shares 28-32.
4. Robert-Guroff M, Schrecker AW, Brinkman BJ, Gallo RC, 1977. DNA polymerase gamma of human lymphoblasts. Biochemistry 16: 2866-2873.
5. Sarngadharan MG, Robert-Guroff M, Gallo RC, 1978. DNA polymerases of normal and neoplastic mammalian cells. Biochimica et Biophysica Acta 516: 419-487.
6. Rey MA, Spire B, Dormont D, Barre-Sinoussi F, Montagnier L, Chermann JC, 1984. Characterization of the RNA dependent DNA polymerase of a new human T-lymphotropic retrovirus (lymphadenopathy associated virus). Biochemical and Biophysical Research Communications 121:126-33.
7. Dourmashkin RR, Bucher D, Oxford JS, 1993. Small virus-like particles bud from the cell membranes of normal as well as HIV-infected human lymphoid cells. Journal of Medical Virology 39: 229-32.
8. Toplin I. Tumor Virus Purification using Zonal Rotors. Spectra 1973:225-235.
Competing interests: None declared