Interesting questions.
I have read that hormones cause certain enteroviral loads (especially coxsackie) - to sky rocket. I understand there is a similar hormonal association with XMRV.
Even if they did not act in concert, a surge in hormonal activity would set them both off - if and when, they are present together in the body. As both are individually nasty (with a capital N) -this would be enough to give rise to the myriad of problems witnessed in ME and CFS patients.
Ok, yet another dumb question from someone who's not a microbiologist, me that is
Can the two types of viruses exchange genetic material as some others can?
could this also be a reason for the effects we have?
Can two viruses belonging to two different families do this? I have no idea either.
I dont know, but I am assuming that a full genome sequence on XMRV was done. So, if what your proposing was possible Sliverblade, (and I have no idea either) -I would have expected some comment to have surfaced somewhere to the effect that human XMRV's genetic structure also resembles in part - that seen in enteroviruses. And given the historical association of ME to enteroviral infection, you would have expected that comment to have surfaced. There is scientific chatter about recombinant strains within XMRV - but that is all, as far as I know.
Having said that, I know that WPI and a laboratory have reported variation in genetic sequences of XMRV - so the question arises - have they done full genetic sequences on all these various strains and if genetic exchange between XMRV (a retrovirus) and an Enterovirus is possible - is it evident in one of these strains?
It is though - a horrific thought.
