There are ways that retroviruses can impact the cell the I believe are especially important to CFS and data exists to support these assertions both in the literature (see below) and in such findings as low SOD and GPx in CFS and provides a mechanism to explain oxygen toxicity by ETM which is nearly universal in CFS.
As for overlap conditions in Dr. Mikovits’ cohort associated with CFS including FM and MCS and chronic Lyme and MS-like patients, I cannot speak to that. However, my clinic is filled with such overlap conditions. I suspect it will not matter very much. They are most likely infected with XMRV if they meet criteria for CFS with or without FM or MCS or chronic Lyme. Perhaps pure FM or pure MCS or pure Lyme will be different in degree of infection and maybe not. It will be very interesting to watch this data develop and expand to CFS-like conditions and the few pure FM and MCS cases that I have seen over the years. I have not really seen what I would call a pure Lyme case but many with CFS and a positive Igenex WB assay and antibiotic failure for chronic Lyme.
Proper buffering of the redox set point for the human body’s biological terrain is critical to control intracellular viral replication. Oxidative stess will potentially amplify XMRV replication. The biggest amplifier of oxidative stress due to any cause is NF Kappa B and one of the best inhibitors of NF-kB are the artemisins (Artesunate and Wormwood). Artemisins are also thought to be useful in cancer. We will be exploring the dose response curve for Artemisins to inhibit infectious XMRV in the near future to determine the best dose. We already know that activating NF-kB activates this virus and suppressing NF-kB inhibits XMRV. Artesunate is also known to inhibit HIV and all the associated herpes viruses that are co-factors in the evolution of AIDS and CFS as well.
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 has been 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.