Well, you seemed to get a lot more out of this than I did.
I got the overall points from it. But the part about the tetherin confused me. I would read the sentence and think it is saying one thing and then I would read it again and think it is saying the opposite.
It used the term "antagonize the tetherin" Does that mean it causes a tetherin reaction or does it mean it prevents the tetherin reaction?
Tina
I think this is good news. Tetherin is a factor that cells produce that appears to stop viral particles from being released thereby rendering them inoperative, if I got that right. HIV has the ability to block tetherin activity but XMRV, a much simpler virus, is unable to do that ('antagonize' tetherin action is a weird way of putting it). She notes that studies have shown that Tetherin can block XMRV activity; at least two antivral cellular factors, then, tetherin and the APOBEC3 G appear to be able to inhibit XMRV in humans.
This could be a little problematic, though. If XMRV is causing damage in CFS then it has to able evade the major antiviral factors... I don't know how many of them there are or where they are but what we really might want to see is XMRV being
immune to a big antiviral factor. We know that the APOBEC 3 enzyme knocks XMRV in the PBMC's tested thus far in the blood - on it's butt. How is a virus that is knocked on its butt going to cause CFS? Either XMRV is flourishing elsewhere in the body in cells that do not have that enzyme or it's doing it's damage without replicating...which I guess is possible ???
HTLV also exists in low numbers and cause damage - so that does happen but it does it by turning cancerous and the research does not yet suggest that XMRV is a cancer causing agent (and of course CFS is not cancer). Still there's alot to learn. Could XMRV be altering the function of immune cells simply by being present in them? I think that's one possibility...