> and also a site that blocks the paracrine mechanism DNA in the neuroendocrine tissue.
Do you know that is, more exactly? You aren't talking about the thing involving cortisol and other hormones, are you? Because that is something different, not related to the integration site.
> But we know from AIDS that damaged immune function does not produce CFS, at least not until the last stage of the disease, and we are not in that situation. So logically doesn't that argue that XMRV must do something else, if it is really pathogenic in CFS? And if it is reliably producing CFS I think that a random disruption is highly unlikely. What do you think?
I don't know. I'm sure lots of AIDS patients have fatigue, but do they all? I donno. HIV is slowing reducing their helper T cell counts, by an unknown mechanism, for a long time. But they don't really get co-infections (or symptoms) until their helper T cell count drops below roughly 200 or 400 or so. I'm sure the threshold varies a little by individual. But before that, they are fine, with maybe a subtle immune deficiency at most.
Because the mechanism of depleting the helper T cells is still unknown, I'm certain it hasn't been uncontroversially connected to anything having to do with HIV's integration.
Proving causality is a very gray area, and HIV itself is a great example. Like most infections, it hasn't satisfied Koch's postulates, whose satisfaction is sufficient but not necessary to prove causation. As a matter of fact, there's really no straight up, extremely simple and rock solid sequence of logic that proves that HIV causes AIDS. But there are so many near-rock-solid clues that the non-causalists are now, justly, very very far out of the mainstream. But you can't just explain it in two sentences, it's complicated and even a summary would take a page or so.
Basically, many studies find EBV in 100% of lupus and MS patients. It's also in almost all healthy people, like, I dono, 95%? So EBV is considered a nice possible cause for those diseases, but faaaaaaaar from certain. But other than that, NO microbe has ever, in all of history, been found in essentially 100% of patients, unless it was so common that it's in most healthy people -- like above 50%. Here we have something that's in essentially 100% of patients, and 26.5 times more common than it is in controls. So yeah, it might not be the cause even if Mikovits et al. is totally confirmed -- but this would be unprecedented. It's hard to say what the chances of this are, other than "not big."