A retrovirus called XMRV is linked to CFS
Recently published in Science (2009) out of the Whitemore-Peterson Institute in Reno, NV along with The Cleveland Clinic and the National Cancer Institute (NIH) is the first convincing association of an isolated retrovirus with CFS. The gammaretrovirus XMRV was only recently discovered in 2007 at the Cleveland Clinic and cultured out of prostate cancer tissue from prostate cancer victims who had a rare mutation in the anti-viral RNAse-L pathway. CFS patients also have unusual alterations in the same anti-viral pathway (1997) though different in its detail and far less rare.
Dan Peterson MD, a long time resident of Incline Village, NV (Lake Tahoe) and I worked for over eight years (1984-1992) to link CFS to a retrovirus. Dan first sent five patient samples to Specialty Labs in 1985 to test for HTLV-1 and 4 of 5 were positive. We did this due to incredible disturbances on flow cytometry of peripheral mononuclear cells producing elevated CD4/CD8 ratios due to CD8 depletion as well as scatter patterns (debris patterns) that the laboratory flow cytometrist said she had only seen in HIV infections. A radiologist at UC San Diego, on review, said our MRI brain scans done on CFS cases showing UBO’s (1988), looked exactly likes AIDS cases. Repeat testing was negative for HTLV-1 and Dr. James Peters of Specialty Labs suggested these CFS patients might have a cross reacting and novel retrovirus that looks like HTLV-1. In 1986, I called the NCI and Robert Gallo MD, head of the foremost retrovirology laboratory in the world at the time, accepted Lake Tahoe samples for a year resulting in the association of an HHV-6A strain with Lake Tahoe CFS cases (1992), only previously linked to HIV infection.
While practicing in Charlotte, NC and based on continued evidence of unusual immune disturbances by flow cytometry including CD4 depletion (ICL) in 15% of CFS patients which was investigated in my clinic and dismissed by the CDC as clinically irrelevant and continued high RNAse-L activity (1994), I contacted Elaine DeFreitas PhD at the Wistar Institute who ultimately found HTLV-II-like genes associated with CFS (1991). Her work was unfortunately assaulted by the CDC that claimed either an endogenous RV sequence that lighted up in cases and controls using her primers (per Dr. J.W. Gow) or null responses to cases and controls (per CDC scientist). Elaine argued that these two scientists with diametrically opposing results manipulated the magnesium concentration which affects the primer stringency and got whatever result they wanted, to make their opposite claims. Her proposal to physically run the assays side by side with the CDC scientists to see if these results could be replicated was dismissed by the CDC. Dr. Gow would later publish his opinions (1992). Left unfunded by senior administrators at the NIH and the CDC, the search for a retroviral link in CFS dissipated and was lost until Judy Mikovits PhD, operating out of the independent Whitmore-Peterson Institutes, revived the long search. I congratulate her and the Whitemore-Peterson Institute.
The finding of antibody or active virus in 95% of CFS and 4% of controls is a result that argues for causality, in my opinion, especially with the associated RNAse-L corruption and NK functional impairment that might predict such an infection. This novel retrovirus could easily shift the redox state just like HIV as published in (2001) and (1995) and induce all manner of associated pathogens as seen in CFS. A redox shift could ultimately corrupt the gut ecology and create P450 decoupling based on NADPH depletion observed in CFS and lead to environmental illness as well. Time will tell but I think Dr. Mikovits is right to suspect causality. I also think this virus is infectious with at least ten million Americans infected who appear healthy and perhaps another four million Americans or more with CFS as recently estimated by the CDC (2007). However, disease expression may be more limited causing the illusion that it is not infectious. Furthermore, there may be other diseases that are similar and dissimilar to CFS that are associated with if not caused by XMRV.
Copyright 2009 - Paul R. Cheney MD, PhD
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