Viruses 2011, 3, 1312-1319; doi:10.3390/v3081312
OPEN ACCESS (full paper can be downloaded)
viruses
ISSN 1999-4915
www.mdpi.com/journal/viruses
Commentary
Origin of XMRV and its Demise as a Human Pathogen Associated with Chronic Fatigue Syndrome
Oliver Hohn and Norbert Bannert *
Center for HIV and Retrovirology, Robert Koch Institute, Nordufer 20, 13353 Berlin, Germany; E-Mail: HohnO@rki.de
* Author to whom correspondence should be addressed; E-Mail: BannertN@rki.de; Tel.: +49-30-18754-2549; Fax: +49-30-18754-2334.
Received: 23 June 2011; in revised form: 4 July 2011 / Accepted: 14 July 2011 / Published: 27 July 2011
Abstract:
Retroviruses are well known pathogens of mammals, birds and fish. Their potential to induce cancer in chickens was already described almost 100 years ago and murine retroviruses have been a subject of study for 50 years. The first human retroviruses, HTLV and HIV, were discovered more than 30 years ago, surprising researchers and physicians by the profound differences in the diseases they cause. HTLV-1 is able to induce, after decades of infection, lymphomas/leukemia or neuroimmune disorders whereas untreated HIV infection leads almost inevitably to AIDS. The recently described XMRV (xenotropic murine leukemia virus-related virus) appeared to possess many of the features known for HTLV and was regarded by some to be the third human retrovirus. However, recent publications by Knox et al. [1] and Paprotka et al. [2] have shed new light on this gammaretrovirus. Knox and colleagues clearly demonstrate that XMRV is absent in patients belonging to a chronic fatigue syndrome cohort who had previously been reported to be XMRV-positive [3]. This supports the growing suspicion that laboratory contamination was responsible for the postulated link between XMRV and the disease. Furthermore, Paprotka et al’s identification of XMRV’s origin and the phylogenetic analysis of known XMRV sequences are further nails in the coffin to the notion that XMRV is a clinically relevant infectious human retrovirus.
Keywords: XMRV; CFS; origin; recombination
The two studies this piece is using as evidence for their argument are deeply flawed.
Knox et al failed to find any evidence, by four different assays, of the VP62 clone of XMRV. Since Knox is heavily invested in HHV6, and since she left the WPI under a cloud, she cannot be considered to have no competing interests. See http://tinyurl.com/3zs2myr
While some scientists, Knox among them, are unable to find HGRV’s, generally because of inadequate or too specific methodology (wild HGRV’s have sequence diversity, all that the assays used by 0/0 studies pick up is the VP62 clone, used to align the primers), many reputable scientist do not have the same problem (1).
Paprotka Coffin and Pathak’s unique recombinant event, that supposedly took place in a hypothetical lab, in tissue of hypothetical lab mice, some time in the early 90s has been bought into question by the work of, among others, Bill Switzer of the CDC (1).
This article is yet another crowd control clone piece. Move along, patients, back to your miserable existence, nothing’s happening here.
1) http://forums.phoenixrising.me/entry.php?959-XMRV-The-case-against-contamination (excellent piece, fully referenced).
The abstract appears to say, “We have done no research. We agree with the other two – therefore they must be right.” Thanks for the history lesson, but history is not scientific methodology?
“This supports the growing suspicion… ”
What about a few facts for a change?