“HIV” has infected virology with cancer-causing viruses

Duesberg (Inventing the AIDS Virus, Regnery, 1996) described in detail how the unsuccessful, decades-long search for human-cancer-causing viruses stimulated frustrated virologists to hunt for and insist on a viral cause for AIDS. That has produced a thriving industry that’s highly lucrative for researchers and drug companies and government agencies and non-governmental entities — albeit unfortunate for millions of healthy and innocent people. That model now seems to be enticing virologists to discover new viruses associated with a variety of conditions, including human cancers, and to market expensive tests to detect those postulated viruses and expensive vaccines to ward them off.

This approach has approval at the highest levels of the scientific establishment, vide the award of Nobel prizes for the discoveries of HIV — which doesn’t case AIDS — and human papillomavirus, HPV — which has not been proven to cause cervical cancer but against which an expensive vaccine has been marketed for administration to teenage girls and more recently teenage boys, who may not be at risk for cervical cancer but still deserve to be protected against genital warts, with which some strains of HPV are sometimes associated (Gardasil and Cervarix: Vaccination insanity, 21 September 2009).

One element of this HIV/AIDS model is that weak associations are declared to be proof of causation: the seminal Gallo papers claimed to find HIV in much fewer than all AIDS patients, and only some strains of HPV are even claimed to be associated with cervical cancer. This betrayal of statistical logic is now exemplified again by the latest retroviral fad, XMRV, xenotropic murine retrovirus, which has been “associated” first with prostate cancer and thereupon with chronic fatigue syndrome, CFS.

First, prostate cancer:
“We found XMRV DNA in 6% and XMRV protein expression in 23% of prostate cancers” (Robert Schlaberg, Daniel J. Choe, Kristy R. Brown, Harshwardhan M. Thaker, and Ila R. Singh. “XMRV is present in malignant prostatic epithelium and is associated with prostate cancer, especially high-grade tumors”. PNAS 106 #38 [2009] 16351-6; doi 10.1073/pnas.0906922106).

In case 6% and 23% seem not too impressive, the authors assert that “Our observations provide evidence for an association of XMRV with malignant  cells and with more aggressive tumors” [emphases added] — in other words, if they could have isolated only the actual tumor cells, of course the association would have been much more impressive. Skeptics might ponder, though, the fact that they “detected XMRV DNA” in 2.0% of controls as well as in 6.2% cases of prostate cancer. We are reminded of Gallo’s decision in patenting an “HIV” test to use 3 times the reading in normal controls as an indication of infection (US Patent 4,520,113, 28 May 1985).

Since HIV has been declared to be an underlying cause in an increasing number of illnesses, obviously any newly discovered virus, especially a retrovirus, ought also to be indictable for an increasing number of ailments. A group of entrepreneurial virologists noted that “XMRV-positive prostate cancer and CFS [chronic fatigue syndrome] have been linked to alterations in the antiviral  enzyme RNase  L” and therefore they looked for XMRV in CFS: “Of the 101 CFS samples analyzed, 68 (67%) contained XMRV gag sequence. Detection of XMRV was confirmed in 7 of 11 [64%] WPI CFS samples at the Cleveland Clinic”( Lombardi VC, Ruscetti FW, Das Gupta J, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Silverman RH, Mikovits JA. “Detection of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome”. Science 326 [2009] 585-9). Finding the putative cause in as many as 2/3 of patients is, by HIV/AIDS standards, more than adequate proof.

A corollary feature of the HIV/AIDS model is that the willingness to accept weak association as causation throws up an increasing number of conundrums. The inference based on “antiviral  enzyme RNase  L” led to the search for XMRV, which is associated with that enzyme, in CFS. Conundrum:     “We found XMRV infection  to  be  independent  of  a  common  polymorphism  in  the RNASEL gene, unlike results previously reported. This finding increases the population at risk for XMRV infection from only those homozygous for the RNASEL variant to all individuals” (Schlaberg et al.).

OOPS! The very reason for looking for XMVR in CFS turns out to be spurious.

Furthermore, other researchers were unable to find XMRV in any appreciable number of CFS patients: “XMRV or MLV sequences were not amplified from DNA originating from CFS patients in the UK” (Erlwein et al. “Failure to Detect the novel retrovirus XMRV in Chronic Fatigue Syndrome”. PLoS ONE 5[1] [2010] e8519. doi:10.1371/journal.pone.0008519).

Now what is one to do when apparent associations turn out to be no association at all? Again HIV/AIDS theory provides a useful model, namely, the conceit that any given illness may look quite different on different continents:
“Although we found no evidence that XMRV is associated with CFS in the UK, this may be a result of population differences between North America and Europe regarding the general prevalence of XMRV infection, and might also explain the fact that two US  groups found XMRV in prostate cancer tissue, while two European studies did not” (Erlwein et al.). “XMRV could show more genetic variety, and thus be harder to detect, than anyone assumed. It’s also possible that distinct strains of XMRV appear in different parts of the world, like the retroviruses HIV and HTLV (a leukemia virus)”  ( Sam Kean, “Chronic Fatigue Syndrome attacked again”, ScienceNOW Daily News, 6 January 2010).

HIV/AIDS provides an apparently unlimited number of good ideas for CFS researchers. Just as there can be AIDS-TB and non-AIDS TB, AIDS Kaposi’s sarcoma and non-AIDS Kaposi’s sarcoma, and so forth, “It’s naïve to think that everyone with chronic fatigue has the same etiology. There’s probably going to be a subset of people with CFS that have XMRV, and it will probably end up being classified as XMRV-related CFS” (Kean, op. cit.).

Another lesson from HIV/AIDS theory and practice is to keep asserting something even if it is not true, thus “We have discovered a highly significant association between the XMRV retrovirus and CFS” (Lombardi et al.). First, the claimed association isn’t highly significant. Second, no association at all has been found by researchers attempting to reproduce the finding. Third, the reason for seeking an association in the first place turns out to be invalid: “As noted above, XMRV has been detected in prostate tumors from patients expressing a specific genetic variant of the RNASEL gene (5). In contrast, in our study of this CFS cohort, we found that XMRV infection status does not correlate with the RNASEL genotype”.

Obviously, the evidence that all this research was based on a flawed hypothesis indicates only a pressing need for more research based on the same hypothesis:
“This observation raises several important questions. Is XMRV infection a causal factor in the pathogenesis of CFS or a passenger virus in the immunosuppressed  CFS  patient  population? What is the relationship between XMRV infection status and the presence or absence of other viruses that are often associated with CFS (e.g., herpesviruses)? [NO ASSOCIATION OF CFS WITH ANY VIRUS HAS STOOD THE TEST OF TIME] Conceivably these viruses could be cofactors in pathogenesis, as is the case for HIV-mediated disease, in which co-infecting pathogens play an important role (20). [Not quite; HIV is supposed to be pathogenic by itself, not requiring co-factors to kill off the immune system — except according to Montagnier, of course.] Patients with CFS have an elevated incidence of cancer (21). [How many other conditions than CFS can be correlated with one or another cancer? Especially if a single unreproduced observation counts as a correlation?] Does XMRV infection alter the risk of cancer development in CFS? . . .  Finally, it is worth noting that 3.7% of the healthy donors in our study tested positive for XMRV sequences. This suggests that several million Americans may be infected with a retrovirus of as yet unknown pathogenic potential”.
Ah, yes.  The 3.7% of healthy people who are XMRV-positive are evidently elite controllers and long-term non-progressors to CFS and cancer. But everyone is obviously at risk, after all this virus MIGHT cause some illness or other — perhaps following a latent period of a decade or two or three? (As Koehnlein pointed out at RA2009, “Life is a sexually transmitted disease which ends in death after an incubation period of 77 years”; briefer incubation periods include HIV at 15 years, HCV 30 years, BSE 55 years,  HPV 55 years).

So just like HIV/AIDS, XMRV is significant for stimulating and supporting researchers, if for nothing else: “virologists around the world practically sprinted to their labs to redo the experiments . . . . a Google search on ‘XMRV’ the day before the Science paper [Lombardi et al.] hit  . . . found about 22,500 hits. Three months later, there are 400,000 hits”( Sam Kean, op. cit.).

Finally (for the moment at least): just as with HIV/AIDS and other unsavory enterprises, FOLLOW THE MONEY:
“the discovery that a clinic associated with the Science paper was selling a $650 diagnostic test for XMRV made the issue more pressing. . . . [S]ome scientists . . . fear that Lombardi’s clinic took advantage of that hunger [for help on the part of CFS patients] by offering the $650 diagnostic test, 300 of which have been administered so far. Lombardi’s group never claimed XMRV caused CFS, so it’s not clear what a patient could do with a positive result. Lombardi argues that patients can avoid infecting other people with XMRV and have their diagnoses validated, if nothing else”.
Great value for $650, for those who sell the tests if not for those who get themselves tested.

Not that any of the researchers admitted to a conflict of interest when they submitted the manuscript to Science (7 May 2009; accepted 31 August). The last footnote did note that “R.H.S. may receive royalty payments in the future from Abbott Laboratories”,  but it was left to a “Note added in proof: V.C.L. is operations manager of Viral Immune Pathologies Laboratory, which is in negotiations with the Whittemore Peterson Institute to offer a  diagnostic test for XMRV”.
Of course, the belatedness of this note, added after the article had been accepted for publication, is really immaterial, because there is little if any precedent for rejecting manuscripts just because of a blatant conflict of interest.

Lombardi may have been too modest in his claims for the benefits of the test. After all, people who are XRMV-positive and who want to guard against all possibilities that it might be harmful can avail themselves of antiretroviral treatment: “websites are abuzz with reports from [CFS] patients who say they have been tested and queries about how to obtain zidovudine (AZT), the antiretroviral drug used to combat HIV. . . . Scientists are . . . warning people . . . of the dangers of dosing themselves with antiretroviral drugs. . . Richard Baker, head of the group that wrote the official UK guidelines on CFS, warns patients against taking AZT, which can have side effects [YES INDEED, AZT CAN HAVE ‘SIDE’ EFFECTS –it causes death, but a side effect is that it kills retroviruses as well]” (Clare Wilson and Ewen Callaway, “CFS patients in UK show no signs of suspect virus”, 6 January 2010).
Still, that doesn’t stop research on using AZT to block XMRV: “In lab experiments reported last month, AZT was found to block replication of XMRV (Virology, DOI: 10.1016/j.virol.2009.11.013)”. “Because XMRV is a retrovirus, it has been suggested that it might be susceptible to some of the many drugs available for treatment of AIDS. Of  ten licensed compounds evaluated for activity against XMRV, just one, AZT (azidothymidine), was found to inhibit viral replication. . . . Because AZT is approved for use in humans, such studies can proceed immediately, without the need for extensive toxicity studies in animals” (Vincent Racaniello, “AIDS Drug AZT Inhibits XMRV”, 091208, citing Sakuma R, Sakuma T, Ohmine S, Silverman RH, & Ikeda Y (2009). Xenotropic murine leukemia virus-related virus is susceptible to AZT. Virology PMID: 19959199).

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We’ve gone full circle: From realizing that there aren’t any human-cancer-causing viruses to establishing by fiat the existence of human-cancer-causing viruses, beginning with cervical cancer which was declared an AIDS-defining disease just because “HIV” — or rather a positive “HIV” test — occurs in some cases of cervical cancer. Nowadays virologists are demonstrating that bits of DNA and protein that  might be parts of some new virus can be found in a whole host of physiological conditions; and they seem willing to establish the existence of a virus simply by inference from those bits and pieces, and to infer the pathogenicity of that imaginary virus from its putative presence in any ailment or unusual physiological condition.

Thus virology has succeeded in mainstreaming junk science.