In a 2 part series I will explain the mechanisms by which XMRV enters human cells, and possible consequences. The cell surface receptors for XMRV have been identified as XPR1 and SYG1: XPR1 is G-protein coupled receptor suspected as a putative progesterone receptor. The first part I will deal with deals with XPR1.
XPR1 is a membrane protein which acts as a signal transducer: it crosses the plasma membrane 7 times. Recently, the structures of a handful of G-protein coupled receptors has been elucidated: Rhodopsin - a visual protein, Beta-adregenic receptor - adrenaline receptor and target for beta blockers, and the A2A adenosine receptor - the receptor our favorite wake up drug caffeine binds to. XPR1 is found in a fairly diverse array of tissues: lymphocytes, hepatocytes, as well as cells in the brain, pancreas, kidney, prostate, and muscle. This is a very important finding indeed.
It is of note that progesterone tends to shift the immune balance towards Th2, and that progesterone levels rise to as much as 10 to 15 times normal during the third trimester. So, as a molecular biologist, it leaves me to theorize that if this virus can mimic progesterone, it can create a state that allows the immune system to ignore the virus, very much like it ignores a developing fetus - scary isn't it? It is also worth noting that mutations in XPR1 bear a strong association with miscarriage, and that such women often bear masculine-like features. Observations reveal that high rates of estrogen, or high rates of testosterone in the absence of progesterone tend to favor the growth of XMRV - progesterone inhibits the formation of DHT. It seems to indicate that succeptibility to ME/CFS is strongly hormone driven, and why ME/CFS and FM are strongly female prevalent.
J. Battini, J.E. Rasko, D. Miller. (1998). A human cell-surface receptor for xenotropic and polytropic murine leukemia viruses: Possible role in G protein-coupled signal transduction. Proceedings of the National Academy of Sciences: