The Perth Group on Etienne De Harven's and Andrew Maniotis's 'unnecessary hypotheses' that 'HIV' is an 'endogenous retrovirus/endogenous retroviral sequence/retroid' – but with which 'unnecessary hypotheses', trying to sound clever and original, they stupidly persist

In November 2009 Professor Etienne de Harven delivered a slide presentation at the Rethinking AIDS conference in Oakland, California, in which he contended that in their 'HIV' discovery paper in Science in May 1983, 'Isolation of a T-Lymphotropic Retrovirus from a Patient at Risk for Acquired Immune Deficiency Syndrome (AIDS)', Montagnier et al. published a micrograph 'unquestionably' showing 'the assembly (budding) of retroviruses on the cell surface of lymphocytes which had been added to the complex cell cultures studied at the Pasteur Institute'.

These 'observed retroviruses', he claimed, were '[human] endogenous retroviruses'.

Such 'HERVs interfere with the interpretation of clinical studies of AIDS patients (Viral load) as well as with the analysis of the original 1983 Pasteur Institute paper'.

In other words, reckons de Harven, Montagnier and colleagues mistook a HERV for HIV.

In a piece posted on the RA website on 19 June 2008, 'PCR for the so-called measurement of HIV viral load', de Harven claimed PCR amplifies 'endogenous retroviral sequences that are present in ALL OF US!', and not 'HIV viral load'.

Apart from having trouble hearing, it seems that de Harven also has trouble reading.

In an email to him and Andrew Maniotis in July 2008 (copied below) the Perth Group pointed out the fallacies of their contentions.

At the RA conference in November 2009, de Harven was still propounding the fallacies the Perth Group had pointed out to him a year and a half earlier.

And his 'PCR for the so-called measurement of HIV viral load' piece – revealing his basic confusion of so-called 'viral load' with 'viral burden' (mentioned below) – is still up on the RA website as the sort of junk science Crowe and his RA go for.

Oh, and Andrew Maniotis is still, in December 2009, emailing everyone about his 'retroids, HERV's, and ... molecular signatures', and suggesting that 'Gallo is on the right track if he revises his hypothesis and if he pursues' them instead. Which is to say, 'HIV' is actually a 'retroid' or a 'HERV' with a unique 'molecular signature'.

What clowns!


From: Valendar Turner
Date: Fri, Jul 18, 2008 at 3:07 PM
Subject: RE: Mr. Duesberg's Soft Spot
To: Etienne De Harven, Andrew Maniotis
Cc: [...]

Dear Andrew and Etienne,

Thank you for your emails.

Unfortunately, although we would very much like to meet with Peter and have indeed requested a meeting to discuss our differences, no such meeting has eventuated or is presently planned.

In your emails you asked us to convey to Peter that HIV is an endogenous retrovirus/endogenous retroviral sequences/retroid. Do neither of you recall the lengthy paper we wrote in Continuum in 1996, before you became dissidents, in response to Peter's claim that HIV had been isolated?  In this paper we presented all possible interpretations of the so called "HIV" DNA/RNA, including its being that of an exogenous retrovirus, and everything you suggest.  This is discussed in detail under the subtitle 6.3. SPECULATIONS ON HIV DNA.  You will appreciate that in 1996 the evidence for any of these possibilities was not as definitive as it is at present.


In your email you refer to an "HIV" molecular signature.  A "signature" as you know, is specific but we do not see anything specific about the so called "HIV" molecular signature.  In fact it's not just its molecular signature that is not specific but everything else about it, particles, proteins, RT and antibodies.


You want us to agree with three propositions.

You say "That measurements of the so-called viral load are never made on isolated retroviral particles (isolated from the blood of HIV+ individuals)".  If by this you mean they should measure the number of RNA molecules in particles isolated from blood then it makes no sense.  Why count molecules to estimate how many particles you have when you can count the particles?

You say "That, instead, these measurements are always made on extracts from circulating leucocyte nuclei".  The viral load is never done using "circulating leucocyte nuclei" or even cells, where most if not all the "HIV RNA" is in the cytoplasm.  Are you confusing "viral load" (RNA in plasma) with "viral burden" (DNA, "provirus")?

You say "That the human genome contains at least 6% of retroviral-analogous sequences".  Could you please define "retroviral-analogous sequences"?

The facts are:

1.    At present there is no evidence that proves the existence of endogenous retroviruses.  This is at least one point of agreement between the Perth Group and Gallo.  During the Parenzee trial, Gallo said a number of times, by definition, a particle can be considered to be a virus if, and only if, evidence exists that it is transmittable.  Responding to a question put to him by Kevin Borick he stated:  "…endogenous retroviruses aren't viruses as your first witness [E.P-E] properly said, they are particles, they have never been transmitted.  A virus is something that infects, that you prove goes from person.  A to B.  Short of that they are particles.  Where a virus at least has to be transmitted in vitro in the laboratory, it goes from one cell to another, it's never been demonstrated for endogenous retrovirus".  (T1298).

2.    To claim that "HIV" DNA is that of an endogenous retrovirus/endogenous retroviral sequences/retroid the minimum necessary but not sufficient condition is to have proof that the PCR primers originate from virus-like particles/endogenous retroviral sequences/retroids.  As far we know no such proof exists.  Do you have proof?

3.     All the HIV experts agree that to prove the existence of the "HIV" genome (RNA/DNA), and proteins, that is, HIV, the particles must be purified.  See attached paper which cites experts testifying at the Parenzee trial.

4.    The ultimate origin of all the primers used to date in "HIV" PCR testing is a poly (A) RNA (adenine-rich RNA) obtained from density gradient material (the 1.16 g/ml band), which Gallo and Montagnier claim to be purified HIV.

5.    Neither Gallo nor Montagnier presented evidence for HIV purification.

6.    In the early 1970s Peter and Gallo showed that retroviral particles contain poly (A) RNA.  But at least Gallo and Temin knew as far back as 1972 that this RNA is not specific to retroviruses.  In 1974 Temin wrote: "The occurrence of A-rich regions in viral RNA has also been used to measure virion concentration [presently known as "HIV" viral load].  Since poly (A) regions are present in many viruses [viruses other than retroviruses] and most messenger RNAs [cellular RNAs], additional criteria for the presence of an rnadnavirus [retrovirus] must be used" [1].

7.    Thanks to the excellent work by Djamel Tahi and the publications of Bess et al and Gluschankof et al we now know that the "purified virus" (1.16 g/ml band) actually consists of nothing but cellular debris.  See attached file Appendix 11 of our Mother to Child Monograph.  This being the case the only scientific deduction one can make, mysterious as it may seem, is that the "HIV" genome is cellular RNA/DNA and has nothing to do with exogenous /endogenous retroviruses or retroids and endogenous retroviral sequences.

8.    Assuming Montagnier and Gallo discovered a virus, its ultimate origin, monkey/ human/ endogenous/ exogenous, while of interest to some, it has no bearing on its transmission and pathogenicity.

The questions are:

1.     Since all the evidence shows that the "HIV molecular marker" is cellular, why should we invoke unnecessary hypotheses?

2.    Since the HIV experts accept that to prove the existence of HIV (genome, proteins), purification is absolutely necessary, and since to date none of them can provide such proof, why do the dissidents give to the HIV experts what they admit they need but do not have?

1. The cellular and molecular biology of RNA tumor viruses, especially avian leukosis-sarcoma viruses, and their relatives, Advances in Cancer Research, Vol 19, pages 47 to 104 (1974).