Dr. Enlanders on the muddled state of XMRV thus far:
I was asked to comment on the XMRV research. In Oct 2009 a virtually unknown Institute in Reno, Nevada, the Whitmore Peterson Institute, published in Science exciting research in which they claimed to have discovered a new relationship between the XMRV virus and CFS/ME. This was exciting news, we hoped it was the initial foundation of proof, that CFS/ME was a physical disease.
Within 6-8 weeks, miraculously, papers were in publication denying the original research. Usually it takes my Medical Center several weeks to allow a research proposal to proceed, followed by several weeks or months for the research to be completed and then several weeks or months for journal acceptance and publication. So I was astounded, as were others, at the time frame of the response, the journals and the relationships of the publishing research centers.
Read more>>:
Doctor Speedy and ME in search of medical honesty
This is written by Cort Johnson, and he tends to get things wrong or leaves out crucial facts. Better to read something else.
ReplyDeleteWhen he says "Like humans their immune cells were able to knock it down with their all purpose XMRV transfiguring APOBEC enzyme.." he is incorrect. We don't know enough yet. All we have seen is that some members of the APOBEC family can reduce XMRV infectivity. There are also studies that show MLV's can evade APOBECC3, 'Murine Retrovirus Escapes from Murine APOBEC3 via Two Distinct Novel Mechanisms', or this study 'The Glycosylated Gag Protein of a Murine Leukemia Virus Inhibits the Antiretroviral Function of APOBEC3'.
Of the studies looking at XMRV one study, 'Apobec 3G efficiently reduces infectivity of the human exogenous gammaretrovirus XMRV', found that "XMRV is resistant to human Apobec 3B, 3C and 3F..."
Another, 'Inhibition of Xenotropic Murine Leukemia Virus-Related Virus by APOBEC3 Proteins and Antiviral Drugs', found "the establishment of XMRV infection in patients may be dependent on infection of A3G/A3F-deficient cells, and cells expressing low levels of A3G/A3F, such as prostate cancer cells, may be ideal producers of infectious XMRV."
And a third, 'Susceptibility of xenotropic murine leukemia virus-related virus (XMRV) to retroviral restriction factors', found "A3G was able to inhibit the infection of XMRV to the same extent as Mo-MLV, more than 200-fold compared with the no-APOBEC control under these conditions. hA3B was also able to inhibit both viruses, but to a lesser extent, only 65- to 80-fold. All other human APOBEC proteins tested, hA3A, hA3C, hA3F (Fig. 2A), and hA3H (Fig. S2) reduced the infectivity of both viruses by less than 10-fold, despite being overexpressed at similar levels to those proteins that restricted infection (Fig. 2B). This result suggests that XMRV is susceptible to restriction by hA3G and hA3B. Although hA3B is poorly expressed in PBMCs (36, 37), hA3G is constitutively expressed..."