We have talked often enough about the blatant plagiarism and history re-writing that seems to be Rethinking AIDS’s most important function these days, but among all the unabashed reinventors of the wheel that constitute its active board members Prof. Etienne de Harven deserves special distinction as indisputably the first among equals. His claim to originality is set forth in his article for the Journal of the American Physicians and Surgeons (JPANDS) called Human Endogenous Retroviruses and AIDS Research: Confusion, Consensus or Science? In connection with this article de Harven makes several related claims, which we have summarised below:
1. Nobody has come up with a satisfactory (alternative) explanation for the detection of “HIV”, especially via PCR, in some people’s blood.
2. Nobody has thought of linking the “HIV phenomena” to so-called endogenous retroviruses, only de Harven has had the scientific insight and imagination to perceive a connection.
3. Nobody has thought of linking Montagnier’s “HIV” EM to endogenous retroviruses.
4. Major claim: de Harven’s brand new dissident idea is that HIV research has been confounded by endogenous retroviruses.
In the introduction to the main topic of his JPANDS paper, the “HIV viral load” test, de Harven cites Eleopulos et al. 1993 as evidence that “the (HIV marker) proteins are most likely cellular, originating from the abundance of cell debris in poorly “purified” HIV samples.” But apparently de Harven has only read half of the paper he cites, otherwise he would surely have noticed the section “Genomic Investigations”, which begins thus:
At present it is generally accepted that “one of the most striking features that distinguishes retroviruses from all other animal viruses is the presence, in the chromosomes of normal uninfected cells, of genomes closely related to, or identical with, those of infectious viruses”80.
Depending on conditions, the provirus genome remains unexpressed or part or all of it may be expressed. The latter may or may not lead to the assembly of viral particles (endogenous retrovirus). 80 In other words, the finding of a viral genome (DNA) or even of RNA, antigens and antibodies to them, is not proof of the presence of infectious particles. Although most of the above findings are from animal experiments, at present, evidence exists that “The human genome carries DNA sequences related to endogenous retroviral genomes that are subdivided into families according to sequence homology. Some are present in only a few copies, whereas others are present in hundreds to thousands of copies”.133 Animal data also shows that new retroviruses may arise by (a) phenotypic mixing; (b) genetic recombination and deletion. When a cell contains two proviruses, progeny may be found that possess the genome of one but the structural proteins of either or both viruses present. Conversely, the RNA may be viral but at least some of the proteins may be cellular. In other instances, the particles do not have a genome at all, or one or more genes are missing (genetically defective viruses). The genetic mixing can be between viral genomes or between viral and cellular genes.80 134 According to distinguished retrovirologists such as Weiss and Temin, new retroviral genomes may arise by rearrangement of cellular DNA caused by many factors including pathogenic processes, a view that proposes retroviruses as an effect and not the cause of disease.135 136 The time and appearance of the viral genome “may be millions of years in germline cells and days in somatic cells”.136 In addition to the above, the retroviral replicative cycle “involves three distinct steps: reverse transcription, DNA polymerization, and the synthesis of RNA from a DNA template (transcription). Any errors made by the polymerase enzyme during the first and the third steps are not subjected to proof reading, the result being pronounced sequence variability”.137 Hence, as long ago as 1973, it was concluded that the above phenomena “will prove a stumbling block to any genetic analysis of RNA tumour viruses”138 (RNA tumour viruses=retrovirus). To date, the data on the HIV genome has not altered the above prediction and shows that many problems may exist with the use of the genomic studies in efforts to prove infection of AIDS patients with a unique exogenous retrovirus.
In this single passage the Perth Group not only express de Harven’s “new idea”, they anticipate and go well beyond his full argument and in much greater depth. The “stumbling block to any genetic analyses of RNA tumor viruses” (so-called endogenous retroviral sequences in the human or animal genomes), which the Perth Group extends to difficulties with proving HIV infection in AIDS patients, is what de Harven clumsily rechristens as “the interference of HERVs in AIDS Research”.
For those who need more examples, here is what the Perth Group asked Peter Duesberg and all dissidents during the Continuum debate in 1995:
Reinhard Kurth, from the Paul-Ehrlich Institute in Germany, and his colleagues, reported that 70% of “HIV-positive patients”, compared to only 3% of blood donors, had antibodies which reacted with the retrovirus HTDV/HERV- K. However, HTDV/HERV-K is not a retrovirus which is present only in AIDS patients, that is, an exogenous retrovirus as HIV is said to be, but HTDV/HERV-K is an endogenous retrovirus or, as Kurth put it, a retrovirus present “in all of us”. How is it possible then to say, based just on an antibody test, that “Montagnier’s strain”, if one assumes Montagnier did isolate such a virus, is not another endogenous retrovirus generated by the conditions present in these patients? [This reference also contains a greatly expanded version of the Perth Group's 1993 discussion on the "HIV genome"]
Since de Harven introduces the Perth Group’s original idea, formulated in different ways in different contexts over the years, unattributed, and even specifically claims it is his own original contribution although he is well aware of the Perth Group’s work, this is plagiarism of the first water. If published under the auspices of a respectable institution, publication or organisation it would have very serious consequences. Needless to say this doesn’t apply to Rethinking AIDS or JPANDS.
De Harven’s biggest difficulty in the paper is explaining why, if “HIV” is a HERV, we are not all positive on the PCR tests, so he simply skips that part and instead muddies the water by informing the reader that:
Human plasma carries various amounts of circulating DNA. Suspected for a long time, this was first demonstrated by modern technologies in 1999, by P. Anker et al., in the blood of cancer patients. (de Harven)
As the title of the study cited by de Harven informs the attentive reader, it was tumour DNA in particular, not “various amounts of circulating DNA”, that was detected by Anker et al. But the question is what relevance does this have to the “HIV viral load”? De Harven continues:
Apoptosis and a large spectrum of infectious diseases are constant components of all clinical AIDS cases. Circulating DNA is expected, therefore, in the plasma of all symptomatic AIDS patients. (de Harven)
Circulating DNA is in fact expected in everybody, as de Harven has just informed us, although the quantity might be higher in cancer or AIDS patients, and the “HIV viral load”, which purports to measure RNA and not DNA, is detectable in the plasma of both symptomatic and asymptomatic HIV positives, so how can de Harven without further ado conclude that, “Retroviral sequences in plasma pellets (is) easily explained by the presence of variable amounts of circulating DNA”? Nowhere does de Harven say anything about possible qualitative differences in the circulating genetic material, instead it is time for another leap of logic:
(O)ne should not, however, expect that these nucleotide sequences would be identical in all cases. Quite to the contrary, since “nucleotide sequences that diverged from co-linearity with the typical retroviral genome (LTRgag-pol-env-LTR) considerably increase the number of HERV families,” the large number of HERV families resulting apparently from frequent recombinational deletions. Expected variations in the observed nucleotide sequences have, unfortunately, often been misinterpreted as an indication for a high rate of HIV mutations! It seems much more likely, however, that the numerous variations in the observed retroviral nucleotide sequences in circulating DNA reflect the large number of HERV families they originate from, and have nothing to do with presumed “mutations” of a hypothetical HIV. (de Harven)
In order to skirt the difficult issue of the “unique HIV genome” and why it is not present in all of us, de Harven simply decides that HIV is not a HERV, but any HERV; the “HIV viral load” detects retroviral sequences indiscriminately whether they belong to the same or even different families of HERVs. If this were the case it would follow that it has never occurred to a single out of the thousands of virologists who have been working with “HIV” that one retroviral sequence couldn’t be just as good as another when it comes to HIV testing. De Harven wants the reader to accept that the virologists who perform “HIV isolation” and who design the nucleic acid test kits use primers that will pick up on anything that’s remotely retroviral, be it DNA or RNA, endogenous or exogenous, from this or that HERV family.
Needless to say, de Harven doesn’t provide a shred of evidence for this claim, and to expose his conceit and the incompetence of an editor who prints this kind of unsubstantiated speculation one need only ask one question: If the virologists can’t tell the difference between “HIV” and the various HERV families that “confound AIDS research”, how do they distinguish between the different HERV families in the first place? Or going back to the original difficulty, if the “HIV viral load” tests are not even specific to any one family of HERVs but react with all of them, why isn’t each and every one of us, or at least all who suffer from illnesses such as cancer, resoundingly positive?
To better understand how wafer thin is de Harven’s and Rethinking AIDS’s grasp of the substance matter, we invite the reader to read Bauer’s blog and especially the mini Q&A session following the post that touts Harven’s article in these optimistic words:
Not much if anything was known about human endogenous retroviruses (HERVs) at the beginning of the AIDS era. By now, a great deal has been found out, and some of it is directly relevant to various conundrums and controversies about HIV. In my opinion, recognition of the existence and characteristics of HERVs offers the possibility of resolving differing views among AIDS Rethinkers, as to whether HIV exists or whether it exists but is harmless. (Bauer)
Firstly, while human endogenous retroviruses is a fairly new field, animal retroviruses had been studied for decades, by Peter Duesberg among others, before the AIDS era. Secondly, the only HERV characteristics that matter in relation to de Harven’s article are that HERVs are 1. viruses 2. “retros” 3. endogenous 4. capable of producing particles 5. able to recombine. Points 1, 2, 3 and to some extent 4 can be learned simply from reading the name “endogenous retrovirus”. Point 5 is not a tautology, but of course it was well known by 1981. Thus, apart from their putative existence in the human genome there is nothing in de Harven’s article about endogenous retroviruses that has not been well known for decades. Zero.
In the Comments thread, the central issue of the HIV genome and its origin was raised by Valerie McClain:
(Quoting Duesberg) “The existence of the retrovirus HIV predicts HIV DNA can be isolated from the chromosomal DNA of infected cells. The prediction has been confirmed as follows: Full length HIV-1 and HIV-2 DNAs have been prepared from virus-infected cells and cloned in bacterial plasmids.” Cloning in bacterial plasmids is a genetic engineering technique. Later in this article Duesberg states, “Thus HIV isolation based on molecular cloning exceeds the old standards defined as ‘Pasteur’ rules by Continuum.” (McClain)
Under ordinary circumstances we would expect Bauer to explain to McClain the exact reason why de Harven has ruled out that “”HIV” is an exogenous virus, but these are not ordinary circumstances:
I do now understand your point. Duesberg is (was?) universally agreed to be expert on retroviruses. Perhaps all of retrovirology used this same sense of “isolation”?
What you cite can still be interpreted in terms of HERVs, it seems to me. To prove exogenous HIV, one would have to show that this “isolation” could NOT be done on a given individual who later became infected which made such “isolation” possible. Since the epidemiolog of “HIV” tests shows that what is being detected is not infectious, either “HIV” is HERV-related or HERV-generated, or the “HIV” tests don’t detect what Duesberg was talking about, which seems unlikely. But I wish a molecular biologist would comment. (Bauer)
Bauer’s answer is as empty as de Harven’s article: First he excuses Duesberg’s deficient understanding of virus isolation by reminding us that Duesberg is an eminent expert in the field. In Bauer’s world eminent experts cannot be expected to be able to follow arguments based on simple logic or understand the meaning of words. Next he all but suggests that Duesberg is a proponent of the HERV theory of HIV, but, presumably because of his superior expertise in retrovirology, he doesn’t understand that what he says can be interpreted in terms of HERVs. Valerie McClain is citing from Duesberg’s second reply to the Continuum challenge about proof of the existence of exogenous HIV. According to Bauer, then, even when Duesberg specifically sets out to prove that HIV is not a HERV, he actually confirms it.
Since Bauer has just informed us that “a great deal has now been found out about HERVs”, the least one would expect is that he is aware that HERVs are not considered to be full length DNA genomes of functional retroviruses; if they were, they would not be described as “fossils’, “remnants”, “defective”. Even the (in)famous “Phoenix” paper from 2006 only claims to establish the theoretical possibility of functional HERVs in vivo:
Human Endogenous Retroviruses are expected to be the remnants of ancestral infections of primates by active retroviruses that have thereafter been transmitted in a Mendelian fashion. Here, we derived in silico the sequence of the putative ancestral “progenitor” element of one of the most recently amplified family—the HERV-K family—and constructed it. This element, Phoenix, produces viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny. We also show that this element amplifies via an extracellular pathway involving reinfection, at variance with the non-LTR-retrotransposons (LINEs, SINEs) or LTR-retrotransposons, thus recapitulating ex vivo the molecular events responsible for its dissemination in the host genomes. We also show that in vitro recombinations among present-day human HERV-K (also known as ERVK) loci can similarly generate functional HERV-K elements, indicating that human cells still have the potential to produce infectious retroviruses.
Keeping this in mind here’s how Duesberg decribes “HIV” in McClain’s reference
HIV has been isolated by the most rigorous method science has to offer. An infectious DNA of 9.15 kilo bases (kb) has been cloned from the cells of HIV-antibody-positive persons, that – upon transfection – induces the synthesis of an unique retrovirus. This DNA “isolates” HIV from all cellular molecules, even from viral proteins and RNA. Having cloned infectious DNA of HIV is as much isolation of HIV as one could possibly get. The retrovirus encoded by this infectious DNA reacts with the same antibodies that cross-react with Montagnier’s global HIV standard, produced by immortal cell lines in many labs and companies around the world for the HIV-test. This confirms the existence of the retrovirus HIV. The uniqueness of HIV is confirmed by the detection of HIV-specific DNA sequences in the DNA of most antibody positive people. The same DNA is not found in uninfected humans.
If Bauer’s considered opinion is that these words are compatible with HIV being a HERV, and that with de Harven and himself as benevolent arbiters all differences between the Perth Group/Stefan Lanka and Duesberg could easily be resolved, why would there be a need for an unspecified molecular biologist to come along and help him out with the central questions? Why didn’t he simply ask de Harven, the author of the article, or Christian Fiala or Gordon Stewart, both credited by de Harven in the published article? They are all sitting on the same board, so it shouldn’t be too difficult.
The answer is this: The piece is plagiarised wholesale from the Perth Group; it is a watered down, distorted, shallow, incoherent reinvention of but one part of their comprehensive analysis, and it is perfectly natural that only the Perth Group themselves possess the depth of knowledge and research to answer all the difficult questions about their own work. Any former dean or professor knows this from experience, but they also know that the plagiarists cannot go to those they have plagiarised, so all they can do is wring their hands, wishing for a deus ex machina molecular biologist to happen along and save the day – when they are not pretending to be too busy and aloof to hear the questions.
Update: Above we asked, “if the “HIV viral load” tests are not even specific to any one family of HERVs, but react with all of them, why isn’t each and every one of us , or at least all who suffer from illnesses such as cancer, resoundingly positive?” De Harven has written a short paper on HIV PCR where the challenge is even more emphatic:
6% or more of the human genome has striking homology with retroviral genome, a fact that is well documented for more than a decade. So, PCR has no difficulty to recognize short retroviral-like sequences in these human chromatin samples (never twice the same, but never mind: it keeps mutating !!), and to amplify it 1000 or million times! Bingo: this is HIV !!!!!! NO: it is the amplification of endogenous retroviral sequences that are present in ALL OF US! It has NOTHING to do with the hypothetical presence of circulating retroviral particles! It has nothing to do with any “measurement” of the “viral load”. By that method, WE ALL have some level of …”viral load”!!! Really? Yes, but to save the establishment from too much embarrassment NO CONTROL, on you and me, was ever made nor published! Do you know the reference of one single paper in which a large group of “normal” individuals would have been studied for HIV “viral load” by PCR measurement? I don’t. (de Harven)
This is a valid point and we are sympathetic to it, but again whence derives de Harven’s certainty? There are in fact large groups of “normal” people who are continually being tested for “HIV” using nucleic acid testing. For instance, babies of HIV antibody positive mothers are likely to carry maternal antibodies for several months, so the PCR tests are considered more reliable than the antibody tests for infants. Not all infants, not even all African infants, test positive on PCR. Likewise, PCR is often used as part of the testing algorithm to confirm the positive antibody result in low risk groups. It would help dissidents greatly if de Harven instead of making unsupported statements in his published papers would deal with specific questions like why are not all babies positive on the nucleic acid tests. Until he faces those challenges we can only conclude that de Harven once more has misunderstood and misapplied what he has misappropriated, namely the Perth Group’s argument that the nucleic acid tests are unspecific and correlate none too well with AIDS or the other “HIV” molecular markers.