EBV and XMRV - a new disease model

An unpublished Spanish study reveals what could possibly unlock the mysteries of CFS.  EBV is a common herpesvirus that almost 95% of the population carries by adulthood according to the CDC, however it seldom produces disease.  In a percentage of the population it causes infectious mononucleosis, but afterwards remains dormant in immune system cells.  It brings the question - Could EBV or another herpesvirus be the key that unlocks the door for XMRV - quite possibly.  Once XMRV enters a cell, it could quite conceivably create an immune dysfunction that allows EBV to reactivate at a low level, fuelling a vicious cycle - through EBV producing a gene that downregulates APOBEC3, somewhat like the HIV vif protein does.

Significance of Co-morbidity of FM CFS/ME and Autoimmune Diseases

The co-morbidity of Fibromyalgia and several autoimmune diseases is well documented in medical literature.  It was accepted for a time that FM CFS/ME were autoimmune disease as well.  It leads me to theorize that many autoimmune diseases are not autoimmune diseases, but rather a consequence of an XMRV-mediated immunodeficiency syndrome.  The finding that the human genome contains many endogenous viral genes that cannot be expressed under normal physiological mechanisms, but can be turned on by certain viruses like EBV, and most likely XMRV makes this a distinct possibility.  So how could this happen?

Many viral proteins are membrane proteins - they embed in the lipid membrane of the virion.  Conceivably, our cells could start expressing these proteins at their surfaces, triggering an immune response.  Many retroviruses contain transcriptional transactivators which there is a strong possibility could accomplish this very event.  It is also conceivable that herpesviruses could work in concert with XMRV to amplify this effect.  An XMRV ravaged immune system in theory can't mount an effective enough response to keep EBV, HHV-6 levels below the "Noise floor".

Ultimately, the significance could be that one viral gene could mean Rheumatoid Artthritis, another could mean Ankylosing Spondylitis, and another could mean Multiple Sclerosis.  This hypothesis could also help explain why what we call autoimmune diseases follow a relapsing-remitting pattern. It could also help prove/disprove the concept of molecular mimicry.