Heinrich-Pette Institute Hamburg: XMRV

Hi,

today I found this project description at the HP-Institute Hamburg:

"Crossing the Species Barrier: Role of Env-Receptor Interactions in Gammaretrovirus Infections

U. Bergholz (1), M. Ziegler (1), K. Stieler (2), A.D. Miller (3), M. Eiden (4), N. Fischer (2), V. Prassolov (5), C. Stocking (1)
(1) Heinrich-Pette-Institute
(2) Universitt-Klinikum-Hamburg-Eppendorf
(3) Fred Hutchison Cancer Center, Seattle, WA USA
(4) National Institute of Health, Bethesda, MD, USA
(5) Engelhardt-Institute of Molecular Biology, Moscow, Russia
The gammaretroviruses compromise a genus of exogenous and endogenous viruses that are widely spread in vertebrates. Analysis of endogenous retrovirus (ERVs) in the genomes of humans, mice, and other species indicates a longstanding association, probably dating back several hundred million years, during which retroviruses have repeatedly colonized host genomes. Phylogenetic studies of class I (gamma and epsilon) and class II (alpha, beta, delta and lenti) ERVs suggest that horizontal transfer of infectious virus between vertebrate classes occurs only rarely, although several important examples have occurred. In addition to the well-known jumping of a lentivirus from chimpanzees (SIVcpz) to humans (HIV-1), a recent report has demonstrated the first bonafide human infection with a xenotropic MLV-related gammaretrovirus (XMRV). Using retroviral pseudotype assays and receptor binding assays, we have demonstrate that XMRV possesses a wide host range and efficiently infects feral mouse cells, as well as established human cell lines and primary cells. Interference assays confirm the classification of XMRV as a xenotropic MLV-like virus, which uses the transmembrane protein Xpr1 as a receptor. Interestingly, XMRV preferentially uses the human versus the murine Xpr1 variant, arguing that XMRV already persists for a longer period in the human population.
Another example of cross-species transfer is the recent characterization of a Koala gammaretrovirus (KoLV), which is currently "invading" the host genome. This virus is closely related to the gibbon ape leukemia virus (GALV), although the vector responsible for transmission of the virus between these two species with distinct habitats has not been conclusively identified. We have recently isolated an ERV from Mus cervicolor, which we have dubbed McERV. McERV is closely related to the GALV and KoLV isolates and thus may share a common ancestor. Host and tissue spectrum analysis has shown that in contrast to most other gammaretrovirus isolates that use ubiquitously expressed membrane transporters as a receptor, McERV uses the myelin protein plasmolipin (PLLP) as a cellular receptor. PLLP expression pattern is restricted to cells of nervous and secretory systems (e.g. brain, spinal cord, kidney, and lungs) and thus retroviral vectors pseudotyped with McERV show tissue expressions. We are currently screening the mouse genome for other uncharacterized ERVs that may shed light on the evolution and spread of gammaretrovirus, but also provide attractive tools for cellular and molecular biology, as well gene therapy."

Although, I don't know whether this is project is still running at the HP-institute, still they make an interesting observation(see in bold). Perhaps others can put this better into context in the light of the latest findings wrt XMRV.

Best regards,
OS.

Thanks for sharing Overstressed.

This appears to be in conflict with more recent opinions strongly expressed by this researcher: A.D. Miller (3) Fred Hutchison Cancer Center, Seattle, WA USA

I'm afraid you won't find a publication with such results. The characteristics of the envelope remain unexplained. It has a functional immunosuppressive domain, it enters cells with human XPR1 receptors, it plays a role in neurological disease. If the virus contributing that env was never in humans its adaptation is a remarkable fluke. We still need to find out where that envelope came from.

Hey daze,(tail wags and paw waves)
Do we know when this was published or even worked on? Cause it appears to be new or newish. Also Fisher is the one who found XMRV in respiratory tracks. So the question here is when was this done? Who is the bonafide human who is infected? How did they establish this bonafide? What is the recent report they are referring too? It's not Fishers Respiratory study because that was totally ignored as we all know.

I'm really curious if anyone can find the date of the report? (eyebrow wiggles)

Hasn't author no.3 been trying to argue the opposite :innocent1:

This was his view back when the paper was written in 2007. Dr. Miller believed this to be the case and the reason for his research between XMRV and ME/CFS. He believe in 2008, 09, 10 that there was a possible connection between XMRV and ME/CFS. The research announced on this forum and other forums was not about whether ME/CFS patients had XMRV, it was about wanting to take it one step further. They accused us of undermining the research of Mikovits that XMRV was associated with ME/CFS. Miller's research was NOT about proving that XMRV was not in ME/CFS patients. However no amount of convincing could prove otherwise. In 2011, his research was to study how XMRV could be a contaminant after the numerous publication of the UK negative research studies.

Even though we stated repeated our research was not to find XMRV or validate or invalidate Mikovits research but to take it one step further. We were researching the effect that XMRV had in patients with ME/CFS. His results of this reseach without the ME/CFS patients were published in the Journal of Virology. His findings concluded if it really existed in humans, XMRV could induce apoptosis of human neuroblastoma cells - presenting a potential mechanism for the neuromuscular pathology seen in patients with chronic fatigue syndrome.

http://okeefe-lab.blogspot.com/2011_11_01_archive.html

Eco