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Nonsense, Insults and Slander: Prof. de Harven Denies Charges of Plagiarism

De Harven did everything possible to indoctrinate people that he has done a great work in the past and now both Duesberg and the PG are wrong and only he is the greatest scientist.  The problem is that in the past the only thing he did was to contribute to messing up cancer research and now he is not even capable of doing a good job as a plagiarist. (The Perth Group, Jan 2012)

Ecco l’articolo tradotto in italiano

In an ongoing email exchange between the two, Steve Stannard directed Prof. de Harven’s attention to our last post and asked him to comment. We feel de Harven’s quite extraordinary answer deserves to be given in full for two reasons. The first is that we wish to give him every possibility to defend himself and show why we are wrong in our assessment of his paper and the second is that his answer illustrates so perfectly the mindset of the Rethinking AIDS orthodoxy.

Good evening Steve Stannard,

I apologize for late answering to your important Dec 29 note!  Sorry!

I must say that I was disturbed by several points in your note, and that’s probably why I hesitated to answer right away!

- I don’t know where Val Turner is finding his quotations, but I can tell you that I NEVER “admitted I never isolated any virus” !!!  To the opposite, for the past almost 50 years (!) I am proud for having achieved an excellent purification of these particles that were present in the blood of Swiss mice suffering from the Friend leukemia. True, at that time, we (Charlotte Friend, Peyton Rous, and me!) were convinced that these viruses were exogenous!  But could you ask Val Turner why he congratulated me in the late 90′s when I reproduced that famous picture in “Continuum”, and why he now seem to feel that this was rubbish!!!   Strange, don’t you think? (I attach that famous picture for your file!!)

- I was well aware about the fact that the PG had reviewed some data concerning endogenous viruses in the 90′s. But this was not their own work, from their own lab!!  They had reviewed OTHER PEOPLE’s WORK, and I don’t see why I should have included their reviews?  When I speak in my JAPS paper about HERVs and about circulating DNA, I carefully quoted Lower (77) and Anker (85) who are real molecular virologist/biologists, WORKING AT THE LAB BENCH!

- The old reviews by the PG (“Speculations on HIV DNA”) do not apply to my JAPS paper at all, because the indisputably NEW IDEA in my paper is for having associated HERVs and circulating DNA, something the PG never alluded to. If you can find any reference in which that critical association is being made before, please let me know!!

- You say that a note Val Turner wrote to me and Andy M. in July 2008 is a clear indication for the fact that Val T. is not ignoring my 2010 paper!!!

Strange, indeed!

- And to give a more recent perspective you sent me that piece by Claus Jensen that has apparently been presented at “The HIV Symposium”!!!

Could you tell me who sponsored that “Symposium”, please ?  Was this a scientific conference? Can hardly believe it!!   It is not enough to put Raphael’s ‘The School of Athens’ on top to make it scientifically valid!! I refuse to believe that Val Turner gives the slightest attention to Jensen’s piece that is an accumulation on non-sense and insults! When I first saw that piece I felt like suing Jensen for slander, but I have better things to do with my time! Val Turner should know that the fact that HIV research has been confounded by HERVs was first claimed, 2008, in Robin Weiss’s lab (C. Voisset’s paper, my ref. 92) and is not MY “major claim” as Jensen quite stupidly stressed!!!

- I verified with orthodox AIDS experts my difficulty to find any evidence for a key missing control, i.e. search for so-called “viral load” in SERONEGATIVE severely ill, non-AIDS patients (not babies, of course !). I corresponded with Jay Levy on that, and he could obviously not find such a reference either… (De Harven to Stannard, jan 2011)

If we take it from the top, the reader will note that de Harven only speaks of Val Turner, as if there were no other members of the Perth Group. We cannot tell if that is because the Perth Group uses Val Turner’s email address, or because he thinks Val Turner is the only Perth Group member worthy of mention, or simply because he has forgotten about the rest. The last explanation seems most likely since de Harven has also forgotten about his own published articles. For instance he informs us, “I don’t know where Val Turner is finding his quotations”. The quotation in question is from a letter by de Harven posted on the Rethinking AIDS website, where he writes:

These famous mouse leukemia retroviruses I have talked about so much (maybe too much!) have always been INTERPRETED as being exogenous, although their contagiousness has never been proved.

Not only has de Harven forgotten that he himself wrote, in support of his “new” theory of HIV, that he never proved the contagiousness (infectiousness) of his leukemia “retroviruses”, it seems that when he made that admission he had also forgotten his original papers where he claimed that the particles he purified were proven to be viruses precisely because they were infectious. This is a quote from the Perth Group’s analysis of de Harven’s early papers:

Since the injected filtrates transmitted “a disease having the character of a leukaemia” (because the filtrates were transmitting the disease especially a malignancy, it does not mean that the filtrates contained a virus, Rous pointed this out in 1911) and the particles were not seen in the nonleukaemic mice, in a paper published in 1960 de Harven and Friend arbitrarily decided to call the particle “virus” particles instead of “virus-like”. “The particles, however, will be referred to as “viruses” and no longer as “virus-like” since all specimens were checked for infectivity and proved capable of transmitting the disease”

The last sentence is a direct quote from de Harven and Charlotte Friend. Since de Harven now claims the particles were in fact not proved to be infectious although the filtrates were capable of transmitting disease where is the justification for calling them viruses instead of “virus-like”?

In terms of the HIV theory of AIDS, if we allow without proof that the non-infectious virus-like particles are endogenous retroviruses, and we also allow that they are capable of transmitting disease, how can we claim that “HIV” (larger than normal quantities of circulating endogenous retroviral DNA and particles, according to de Harven) is harmless?

In the last paragraph of his letter to Steve Stannard de Harven writes:

- I verified with orthodox AIDS experts my difficulty to find any evidence for a key missing control, i.e. search for so-called “viral load” in SERONEGATIVE severely ill, non-AIDS patients (not babies, of course !). I corresponded with Jay Levy on that, and he could obviously not find such a reference either…

De Harven is alluding to our and Duesberg’s observation that if “HIV” were an endogenous retrovirus, it would per definition be part of the human genome and the PCR tests should be able in principle to detect it in all of us. We wrote previously that we think de Harven has a good point about the lack of controls for the “HIV viral load”, but since de Harven defines “HIV” as any circulating endogenous retroviral DNA the question remains, why is it not detected more often for example in babies – even seropositive babies (babies of HIV positive mothers typically retain maternal antibodies for several months, which is why the PCR tests are considered more reliable for infants)? De Harven himself is in full agreement with the point that even “normal individuals” should be positive on the viral load tests:

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 on RA site)

De Harven has now redefined “normal individuals (like) you and me” as “severely ill non-AIDS patients”, and further that babies “of course” do not qualify. A contradiction? Not exactly. Finding himself under pressure, de Harven has merely “borrowed” another point from the Perth Group, that the sequences defined as “HIV” often seem to arise as the result of pathological processes, or at least uncommon conditions, which is why they are in fact not present in all “normal individuals”.  If de Harven now admits that his “HIV” can only be found in severely ill people, he has also admitted that it is per definition not a human endogenous retrovirus, which is part of all of us all the time, although perhaps not at all times circulating at detectable levels in the bloodstream.

This brings us to de Harven’s defence against our plagiarism charges, which was the following:

Could you tell me who sponsored that “Symposium”, please?  Was this a scientific conference? Can hardly believe it!!   It is not enough to put Raphael’s ‘The School of Athens’ on top to make it scientifically valid!!

The readers will recognise the empty snobbery that has now become the standard reply by any Rethinking AIDS board member to any challenge or inquiry: they don’t need to consider it if it is not published in a scientific journal. De Harven’s response goes even further in saying that a plagiarism charge against claims published in marginal publications like JPANDS or on the Rethinking AIDS website must have a scientific sponsor to be valid. The same sentiment was expressed by Marco Ruggiero recently in a reply to our critique of Duesberg’s rehashed Medical Hypotheses paper:

All the considerations written by Chris Rawlins and Claus Jensen are interesting indeed. I have a suggestion; why don’t you publish them in a peer-reviewed scientific journal indexed in PubMed? Or, alternatively, why don’t you present them at some International Scientific Congress on AIDS? It is not difficult, I guarantee; Prof. Duesberg, Bauer and myself have done it hundreds of times. If you need an academic affiliation, I can easily provide you with a temporary one. Publishing will make your considerations much more valuable for the entire scientific community. (Ruggiero, Jan 2012)

Readers familiar with our post “PubMed Bagging with Bauer and Ruggiero” may be excused for thinking that this is voluntary self-satire, but rest assured there is nothing voluntary about it, Ruggiero truly believes it is a knock-out argument that a critique of an unpublished (or recently published at the time) paper has not appeared in a scientific journal.

To see how empty is de Harven’s and Ruggiero’s conceit one merely has to look at their response when the analysis or rebuttal does appear in a scientific publication. First de Harven on the same plagiarism charge:

- I was well aware about the fact that the PG had reviewed some data concerning endogenous viruses in the 90′s. But this was not their own work, from their own lab!!  They had reviewed OTHER PEOPLE’s WORK, and I don’t see why I should have included their reviews?  When I speak in my JAPS paper about HERVs and about circulating DNA, I carefully quoted Lower (77) and Anker (85) who are real molecular virologist/biologists, WORKING AT THE LAB BENCH!

What to do when the proof of one’s plagiarism fulfills the arbitrary criterion of having been published in a scientific journal? Easy, one simply raises the bar in an equally arbitrary manner. Now review articles don’t count, only the work of “real virologists/microbiologists WORKING AT THE LAB BENCH!” Once again we are reminded of Ruggiero’s boast that he is a real scientist because he works in a real lab while others “just talk” (Ruggiero has apparently forgotten that his proudest inspiration, post-modern philosopher and charlatan Jaques Derrida, also “just talked”), but even more so of Duesberg’s reply when Joyce Arthur asked him why he hadn’t replied to a published rebuttal of his Medical Hypotheses paper in the journal AIDS and Behavior.

The new Essex paper on “denialism” is, however, from without my professional expertise and published in a journal that deals with “behavior”.  Neither “denialism” nor “behavior” are within my current professional expertise.  Instead I am a scientist dealing with facts and hypotheses and theories.  Once the original scientific debate is settled in a scientific journal, I might, however, try to take a course on “denialism” and “behavior” in order to understand whether this is relevant to science. (Duesberg to Joyce Arthur Dec. 2011)

Duesberg is seemingly unaware that there is such a thing as a science of behaviour, at least as “hard” as his favourite hobby, epidemiology, that deals with facts and hypotheses and theories. But even if he were aware it surely wouldn’t qualify in his view, since science is something one does at the “LAB BENCH!”

The ignorance and conceit on display in these standard replies to anything perceived as being less than pure hero-worship is self-defeating for a variety of reasons, but chiefly because no dissident, per definition, is impressed with such answers, similar in every particular to the excuses given by the Orthodoxy for not engaging with critics. By using this line of argument Duesberg et al. self-identify as anti-dissident. They also self-identify as contemptible hypocrites since their own blogs and websites are full of complaints about the peer-review system, defences against allegations of practicing pseudoscience and of their own (lack of) credentials, the right to have their papers judged on the merits, calls for open debate in any forum, etc.

We have shown previously how the Rethinking AIDS board with Crowe as president, Duesberg as the chief scientist and Bob Leppo as the financial backer has become a perfect microcosm of the corrupt, interest-conflicted intertwining of money, science and politics they claim to oppose. With Ruggiero in the picture it has now also become a perfect microcosm of the members only cronyism that characterises the HIV/AIDS establishment. Ruggiero’s false boast about having done it “hundreds of times” notwithstanding, publishing dissenting papers about HIV and AIDS is nearly impossible even for those with permanent academic affiliations, impressive formal credentials and good connections. As Duesberg himself tells everybody who can be bothered listening, he tried several other journals, including the bottom-ranking JPANDS, before finally having to settle for the unlikely Italian Journal of Anatomy and Embryology (IJAE), which by strange coincidence happens to be published by Marco Ruggiero’s academic affiliation, the University of Firenze. By another strange coincidence, the “hundreds” of international scientific congresses on AIDS attended by Ruggiero, Bauer and Duesberg since Ruggiero became a board member were also Italian affairs if not directly hosted by Ruggiero’s university.

Significantly, all successful submissions for IJAE and scientific congresses (actually no more than a handful) by Bauer and Duesberg list Ruggiero’s students and co-workers from the University of Firenze as co-authors. Daniele Mandrioli and Ruggiero himself magically became distinguished “co-authors” on Duesberg’s latest paper, the earlier versions of which they had nothing to do with, by adding these three random Italian tidbits:

Almost identical figures have been reported recently for Italy, where AIDS is also still restricted to the original risk groups and paediatric AIDS is virtually non-existent (Ruggiero et al., 2009).

Similar non-correlations between mortality and prevalence of HIV were found in Italy. The Italian case is, however, based on actual data rather than on estimates (Ruggiero et al., 2009).

And a recent Italian study reported that the high toxicity of early anti-HIV treatment was responsible for the death of 2000 AIDS patients in 1997 (Ruggiero et al., 2009).

The co-authorship of other people on the list has left even less of a trace. And that is all quite in order. While it might occasion a quiet smile, one dissident should not begrudge another these “Trojan horses”, publishing in obscure journals, edited by friends and close colleagues, under laughable pretenses of relevance to anatomy and embryology, or the artificial ways of padding author lists and résumés. We all know that no other avenue is open, and the Orthodoxy sustains itself on this kind of mutual favours and back-slapping so why should dissidents deny themselves the opportunity when it arises? However, crowing about it in this way, ridiculously exaggerating one’s mainstream bona fides in order to mock or impress fellow dissidents once again reveals the mindset and the spirit of Rethinking AIDS as profoundly anti-dissident.

A little known fact, little known because it should not matter among dissidents, is that at least three of the Rethinking AIDS JPANDS publications, two by Bauer, one by Duesberg, were sent to the Perth Group for review. In the case of Duesberg’s paper the Perth Group referred JPANDS editor L. R. Huntoon to the critical analyses on the TIG site – ironically the same analyses Ruggiero believes are of no value because they haven’t been PubMed indexed. That alone, disregarding the Perth Group’s entire scientific corpus, would have been enough by Rethinking AIDS board standards to earn TIG members a co-authorship of the latest version of Duesberg’s paper. But the reality is that for dissidents to achieve “hundreds” of co-authorships the only important qualification at the moment is to be in Ruggiero’s and Duesberg’s good book.  That is the very definition of the corrupt mainstream cronyism Rethinking AIDS pretends to be opposed to.

Returning to de Harven, we readily see how the practice of quoting the Perth Group as authorities, even seeking their advice and opinion one moment only to turn around and mock them for not being real scientists the next, plays out. De Harven is seemingly oblivious to the fact that the 1993 paper by the Perth Group he thought was too amateurish to reference on the origin and nature of HIV DNA is the same paper he references as authoritative if not definitive on the origin of the HIV proteins:

The considerable difficulty in isolating and purifying HIV was recognized, as early as 1993, by Eleni Papadopulos et al., who correctly concluded that without successful HIV purification, the retroviral nature of the “HIV marker proteins” was most uncertain. Papadopulos emphasized that these proteins are most likely cellular, originating from the abundance of cell debris in poorly “purified” HIV samples.  (de Harven, JPANDS, 2010)

By applying his wholly arbitrary criteria of scientific validity in this wholly arbitrary manner to qualify and disqualify the Perth Group as circumstances dictate de Harven can now claim that Robin Weiss in 2008 was the first to point out that so-called endogenous retroviruses confound HIV research, because, although the Perth Group already explicitly reached that conclusion in 1993, they’re only real, quote-worthy scientists when it concerns the HIV proteins.

There is only one problem with this, nowhere in the cited paper do Weiss et al claim that HERVs have confounded HIV research. They do claim that HERVs are confounding factors for human retrovirus discovery, but nowhere do they claim that this applies equally to the already discovered HIV. We expect, however, that this is only a minor difficulty for de Harven, since to him the important thing is that he can quote a real lab bench scientist, even if the quote is made up.

Since de Harven now has credited the no doubt grateful Robin Weiss with the “new idea” that HERVs have confounded HIV research, what is his own contribution? According to himself it boils down to this:

the indisputably NEW IDEA in my paper is for having associated HERVs and circulating DNA, something the PG never alluded to

In other words, if the human genome is made up to any degree of HERVs a corresponding fraction of circulating human DNA will reflect this, and the viral load tests will pick it up. As has been pointed out to de Harven many times, he is indeed the first to present the “NEW IDEA” that the viral load tests detect retroviral DNA, since every “real lab bench scientist” stupidly insists that the viral load detects RNA rather than DNA. If de Harven could be persuaded to indulge all those scientists who perform viral load measurements on circulating endogenous RNA rather than DNA, he will be able to find plenty of references to prove that the association between HERVs and circulating RNA has long been assumed as a matter of fact. This 2006 paper, chosen at random, discusses the link between “HIV” infection and HERV expression as measured by the viral load test. It is hard to imagine how the paper could have been conceived and written if it were not established as a matter of fact that HERVs and circulating RNA are “associated”, and indeed that “HIV infection” and HERV expression are associated – although, according to de Harven, these researchers should not have been able to distinguish between HIV and HERV-K in their viral load tests.

Logically speaking, if the nucleic acid tests don’t pick up on a unique exogenous retrovirus, what could they possibly be picking up on but circulating cellular material? De Harven’s “NEW IDEA” is to point out that if you believe a part of the human genome consists of so-called HERVs, you naturally also believe that some of the cell-free cellular material will consist of such HERV fragments. If, like Dr. Maniotis, you correctly leave out the virus part of “retrovirus”, you will associate the viral load tests with circulating “retroids”. If, like the Perth Group, you don’t agree with calling these genomic elements viruses or retroids, then of course you will not explicitly associate HERVs with circulating RNA/DNA, you will most often simply call it cell-free cellular material. The point is almost too trivial to make, certainly too trivial to warrant a scientific paper based on it.


4 Responses to “Nonsense, Insults and Slander: Prof. de Harven Denies Charges of Plagiarism”

  1. Gene Semon says:

    Claus, what you chose “at random” on HERV “viral load” is interesting because this same group teamed up with Markowitz at the University of Michigan to produce a paper that should interest all dissidents, especially Peter Duesberg.

    Apparently, cancer researchers are back to retrovirus + oncogene research, notwithstanding Peter’s extraordinary 3 papers of the eighties. So one might think he should simply leave epidemiology in the hands of people like Chris Rawlins and defend his real legacy, now being challenged once again. (Of course, he may have responded to the paper below and we’d love to know about that.)

    What’s fascinating, I think is this statement from the paper confirming Professor deHarven. “It is generally very difficult to detect pathogenic viral particles in the blood of patients by EM; for example, this has never been done successfully with HIV-1-infected patients.”

    Contreras-Galindo et al; Human Endogenous Retrovirus K (HML-2) Elements in the Plasma of People with Lymphoma and Breast Cancer. J. Virol. October 2008 vol. 82: 9329-9336

    “Here we show that RNA from human endogenous retrovirus K (HERV-K) (HML-2) … can be found in very high titers in the plasma of patients with lymphomas and breast cancer as measured by either reverse transcriptase PCR or nucleic acid sequence-based amplification. Further, these titers drop dramatically with cancer treatment. We also demonstrate the presence of reverse transcriptase and viral RNA in plasma fractions that contain both immature and correctly processed HERV-K (HML-2) Gag and envelope proteins. Finally, using immunoelectron microscopy, we show the presence of HERV-K (HML-2) virus-like particles in the plasma of lymphoma patients. Taken together, these findings demonstrate that elements of the endogenous retrovirus HERV-K (HML-2) can be found in the blood of modern-day humans with certain cancers.

    HERV-K (HML-2) has been linked to oncogenesis. Indeed, this virus first came to the notice of biologists due to its similarity to mouse mammary tumor virus (MMTV), a virus that causes mammary tumors in mice, replicates in lymphocytes, and has an exogenous phase and an endogenous phase. Consistent with the similarity of HERV-K (HML-2) to MMTV, HERV-K (HML-2) env has been found to be overexpressed in breast cancer tissue, where it also exhibits novel, alternatively spliced forms.

    HERV-K (HML-2), which has two forms, type 1 and type 2, can encode at least two putative oncoproteins. Type 1 encodes the newly identified Np9 oncoprotein, whereas type 2 encodes an accessory protein, Rec, which is necessary to export unspliced RNA from the nucleus to the cytoplasm like its counterparts human immunodeficiency virus type 1 (HIV-1) Rev and human T-cell leukemia virus type 1 Rex. Both Np9 and Rec have been shown to be capable of cellular transformation under certain circumstances, and Rec can induce carcinoma in situ in mice.

    We recently made the observation that HERV-K (HML-2) RNA can be found in the plasma of HIV-1-infected patients (18, 19). In view of this and the factors cited above, we investigated whether HERV-K (HML-2) RNA might also be present in the blood of patients with either lymphoma or breast cancer. We report that these patients indeed have extremely high titers of viral RNA in their blood, and these titers fall precipitously when patients are treated for lymphoma. We further demonstrate that individuals with lymphoma who have high titers of HERV-K (HML-2) RNA also have reverse transcriptase activity and viral Gag and Env proteins in the same plasma fractions in which viral RNA is found. Finally, using electron microscopy (EM) and immunogold staining we visualized, for the first time, the presence of HERV-K (HML-2)-like particles in the plasma of people (lymphoma patients). These findings demonstrate that HERV-K (HML-2) viral elements can be found circulating in the blood of humans with lymphoma and breast cancer. “

    Not virus-like elements but “viral elements”, which apparently are more “there” than HIV! So much for Gallo’s testimony at Parenzee too.

    So I for one shall take a break, study this fascinating article and compare it with the good professor’s JPAND’s paper before I return.

  2. Gene Semon says:

    Sometimes one has to look backward in order to move forward. I’ve taken the time to present an excerpt of an old paper, not only for Professor deHarven’s benefit, but as a cautionary to the authors of the J of V paper above. Surely this is not the time for the “proximate cause” fallacy to guide research into cancer and AIDS once again.

    The current controversy over the ultrastructural interpretion of retrovirus-like particles is not without precedent. Way back in the sixties “real scientists” were trying to distinguish “elementary bodies” of mycoplasma from “animal leukemia viruses”. At that time, it was most certainly progress when researchers like Peter Duesberg did nucleic acid typing (fractionation/sedimentation to the 70S band/RF tagging) to distinguish “retroviruses” from everything else.(1)

    Here’s the section “Electron Microscopy Studies” from (2):

    “Ultrastructure of Animal Leukemia Viruses. The leukemia and lymphoma viruses of chickens (Ellerman et al, 1908; Purchase, 1965) as well as those of mice and rats (Gross, 1951, 1964; Maloney 1964) have been studied extensively. The morphology of the various leukemia viruses is similar (see review by Anderson, 1965; Zeigel et al, 1964): (1) In thin sections of infected cell cultures or animal tissues, the virus develops by bud-formation at the surface of the cell (Anderson, 1965; deHarven and Friend, 1960, 1964; Dalton et al, 1961, 1964b). The mature virus particle (seen outside the cell in the extracellular spaces), is about 100 mu* in diameter and is characterized by a dense nucleoid and an irregular outer membrane with an occasional tail-like protrusion (extension). (2) In negative staining preparations of mouse-leukemic plasma pellets, the mature virus particle appears to be more electron-lucent, and the tail-like protrusion is more common (Dalton et al, 1962, 1964a).

    Virus-like particles in Clinical Materials. Virus-like particles were found in: (1) The plasma and bone marrow tissues of patients with leukemia (Dmochoski et al, 1959; …); (2) Lymphoma tissue from Africans (…); (3) Lymphoma tissue from Americans (…); (4) Bone marrow of persons with multiple myeloma (…); and (5) Plasma of persons clinically diagnosed as having infectious mononucleosis (…). Some of these particles appeared myxovirus-like (…); some herpes virus-like (…); and some were morphologically similar to avian and mouse leukemia viruses (Porter et al, 1964).

    Virus-like particles have been found in the milk of apparently healthy humans and cows (…), in the milk of cows with a high incidence of lymphosarcoma (…) and were implicated in the etiology of bovine leukemia (…).

    Ultrastructure of Mycoplasma. Cell cultures infected with mycoplasma as well as broth cultures of these organisms contain structures which are morphologically similar to the virus-like particles in the neoplastic tissues. Some of the structures seen in cultures containing mycoplasma have spherical bodies with tail-like protrusions morphologically similar to the virus-like particles described in neoplastic tissues. Some of the structures seen in cultures containing mycoplasma have spherical bodies with tail-like protrusions morphologically similar to the virus-like particles seen in plasma pellets from persons with leukemia (…). Some mycoplasma have bud formation (Figure 1) which may resemble the virus-budding of mouse leukemia viruses (Anderson, 1965; …), while others have a myxovirus-like appearance.”
    Figure 1 caption: “Budding of elementary bodies of Mycoplasma hominis, type 1, strain HEp-2 (D.R. Anderson, Wistar Monograph No 4), x 100,000.”

    “Thus, on the basis of electron microscopic studies, mycoplasma and true animal leukemia viruses possess certain structural similarities. The particles seen in human neoplastic tissue may represent mycoplasma and/or viruses. The investigator searching cell cultures and other tissues for microbial agents by means of electron microscopy should be familiar with the ultrastructure of mycoplasma and should respect the limitations of this useful procedure for the identification of microbes.”

    Excerpted References:

    “Anderson, D.R. 1965. Subcellular particles associated with human leukemia as seen with the electron microscope. In Methodological Approaches to the Study of Leukemias. V. Defendi (ed.). The Wistar Press, Philadelphia: 113-146

    Dalton et al. 1961. An electron microscopic study of a series of murine lymphoid neoplasms. J. Nat. Cancer Inst. 27: 747-791

    Dalton & Moloney. 1962. Recovery of virus from the blood of rats with induced leukemia. In The Intrepretation of Ultrastructure. R.J.C. Harris (ed). Academic Press, New York and London. 385-392

    Dalton et al. 1964a. Studies on murine and human leukemias. Trans. Assoc. Am. Phys. 77: 52-63

    Dalton et al. 1964b. Further electron microscopic studies on the morphology of the Moloney agent. J. Nat. Cancer Inst. 33: 255-275

    deHarven & Friend. 1960. Further electron microsopic studies of a mouse leukemia induced in cell free filtrates. J. Biophys. Biocehem. Cytol. 7: 747-752

    deHarven and Friend. 1964. Structure of virus particles partially purified from the blood of leukemic mice. Virology 23: 119-124

    Dmochowski et al. Studies on human leukemia. Proc. Soc. Exptl. Biol. Med. 101: 686-690

    Ellerman & Bang. 1908 Experimentelle leukamie bei hunhern. Zentr. Bakteriol. 46: 595 -609

    Gross L. 1951. “Spontaneous” leukemia developing in C3H mice following inoculation in infancy with AK-leukemic extracts, or AK-embryos. Proc. Soc. Exptl. Biol. Med. 76: 27-32

    Gross L. 1964. How many different viruses causing leukemia in mice? Acta. Haemat. 32: 44-62

    Moloney , J.B. 1964 The rodent leukemias: Virus-induced murine leukemias. Ann. Rev. Med.: 383-392

    Porter et al. 1964. Association of electron-dense particles with human acute leukemia. J. Nat. Cancer Inst. 33: 547-556

    Purchase, H.G. 1965. Rous Sarcoma and its helper viruses. (A review). Avian Dis. 9: 127-145

    Ziegel et al. 1964. Comparative morphologic and biologic studies of natural and experimental transmission of avian tumor viruses. In Avian Tumor Viruses. J.W. Beard (ed.). Nat. Cancer Inst. Monograph No. 17: 711-731”

    *nm in current lingo

    Thus, clearly a reasonable person can draw the conclusion, even away from the lab bench, that confounding by mycoplasma cannot be ignored by “the investigator searching cell cultures and other tissues” for retroviruses “by means of electron microscopy”.

    1. Duesberg and Robinson (1966) PNAS – (will dig out detailed ref – next post)

    2. Michael F Barile; Mycoplasma and Leukemia. (July 28, 1967) Ann NY Acad of Sci. V143, 557

  3. Gene Semon says:

    As promised, here are some details from reference 1 above. It seems to me that one can say as a first response to Professor deHarven’s Continuum EM “very nice pictures” but on further scrutiny based on below paper, one can say, “clearly you didn’t go the distance”.



    “The viral etiology of several mouse leukemias has been firmly demonstrated. The biological effects of these viruses have been studied extensively, but little is known about their molecular structure. It is known, however, that the mouse leukemia viruses have several structural properties in common with the avian tumor
    viruses and with the myxoviruses. Their viral nucleic acid is RNA. They contain a significant amount of lipid making them disruptable by ether, and making their buoyant densities less than those of nonlipid-containing viruses. They have similar sizes and similar dense staining inner cores with less dense double outer
    “membrane” structures in electron micrographs. However, nothing is known about the size and structure of the RNA in the mouse leukemia viruses. Obstacles to such studies have been the difficulty in obtaining large quantities of purified virus and the inability to extract intact RNA from the virus.”

    “(T)he sedimentation properties of intact MLV-RNA were studied in the Spinco model E analytical ultracentrifuge using W-optics. This experiment was done with a minimum of RNA because of the limited amount of material available. MLV-RNA was obtained by purification of virus from 90 ml plasma from leukemic BALB/c mice. The total fast-sedimenting RNA recovered after sucrose gradient fractionation (as shown in Fig. 2) was about 20-30 ug.”

    “No single-stranded RNA with a sedimentation constant as great as 74S has been previously described. The avian tumor viruses, RSV + RAV and AMV, were recently shown to contain RNA’s with a sedimentation constant of 71S. Thus, avian tumor viruses and the Rauscher virus contain single-stranded RNA’s of similar size, and these RNA’s are probably larger than the known single-stranded RNA’s from other groups of viruses.”

  4. Gene Semon says:

    Claus, Etienne has responded (via email to me) to this part of your post:

    “As has been pointed out to de Harven many times, he is indeed the first to present the “NEW IDEA” that the viral load tests detect retroviral DNA, since every “real lab bench scientist” stupidly insists that the viral load detects RNA rather than DNA. If de Harven could be persuaded to indulge all those scientists who perform viral load measurements on circulating endogenous RNA rather than DNA, he will be able to find plenty of references to prove that the association between HERVs and circulating RNA has long been assumed as a matter of fact.”

    It’s by way of sending this paper for my consideration:

    Salimnia et al; Discordance between Viral Loads Determined by Roche COBAS AMPLICOR Human Immunodeficiency Virus Type 1 Monitor (Version 1.5) Standard and Ultrasensitive Assays Caused by Freezing Patient Plasma in Centrifuged Becton-Dickinson Vacutainer Brand Plasma Preparation Tubes. J. Clin. Microbiol. September 2005 vol. 43 no. 9 4635-4639 http://jcm.asm.org/content/43/9/4635.full

    “Since the viral load assay employs reverse transcriptase PCR technology, it can amplify any virus-specific template, either DNA or RNA, that may be present. A recent study by the Viral Quality Assurance Laboratory (NO1-AI-85354) determined that a single copy of HIV-1-specific proviral DNA could increase the detected viral load by 100 to 200 RNA copies (Cheryl Jennings [Rush Medical Center], personal communication).”

    Thus the JPANDS paper is also confirmed (as noted in my first post of 2/3/12 abv) in this latter regard, given the facts of apoptosis as a protective response against pathological process.

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