Here are a couple more interesting articles showing how the mouse version of XMRV works... Again, take my summaries with a grain of salt. I could have some aspect of the science wrong B Lymphocyte Activation by Coinfection Prevents Immune Control of Friend Virus Infection1 - http://www.jimmunol.org/cgi/content/abstract/181/5/3432 In this one they found that even if a mouse would normally have the genetic ability to resist the virus if they first caught a different virus (LDV) they wouldn't be able to stop the retro-virus from infecting them. In humans this could explain the disease clusters. If some other virus acted as a helper for XMRV (One of the various ones people thought was the root cause over tha last 20 years) it could have an outbreak in an area followed by those who were infected by XMRV getting CFS. Immune Control and Prevention of Chronic Friend Retrovirus Infection http://www.bioscience.org/u37153137/gaDTRQo7632rgysaGWQYT64356/2007/v12/af/2167/2167.pdf This one describes the battle between the immune system and the related mouse retro-virus. How the virus escapes sounds similar to XMRV. Race between Retroviral Spread and CD4+ T-Cell Response Determines the Outcome of Acute Friend Virus Infection http://jvi.asm.org/cgi/content/full/83/21/11211 This article kind of summaries the top two. Interestingly, it seems like the immune system dysfunction described seems to mirror what happens in people with CFS. http://jvi.asm.org/cgi/content/full/83/21/11211 Here is an interesting summary from that article "As with other retroviruses, FV establishes persistence and causes disease in virus-naive mice, in spite of the induction of a virus-specific primary immune response, and this ability of FV is amplified by additional genetic susceptibility or by coinfection." It would be intersting for someone to contact 23andMe and see if we could use their system over time to find the genetic variation in something like MET that is causing the susceptibility to XMRV.