XMRV: Necessary but not sufficient?

[Guest guest]

Hi, all.

It seems to me that the information currently available on XMRV suggests that it

is necessary, but not sufficient, for a person to be infected with XMRV in order

to develop ME/CFS.

I say " necessary " because nearly all the people who had ME/CFS were found to

have this infection.

I say " not sufficient " because a significant percentage of the healthy controls

from the general population were also infected, but had not developed ME/CFS (at

least not yet!).

I think that the only way we can interpret this combination of observations is

to say that XMRV is " necessary but not sufficient. "

If XMRV infection is not sufficient alone to produce a case if ME/CFS, what else

would be needed? I don't think that's known yet. It could be that other

infections are needed, or it could be that the immune system must be

compromised.

As far as I can tell, the latter would be compatible with the GD-MCB hypothesis,

which proposes that a variety of stressors (physical, chemical, biological

and/or psychological/emotional) raise cortisol and epinephrine and place demands

on glutathione, tending to lower it, before the onset of ME/CFS.

Lowering glutathione produces oxidative stress, and the virus apparently needs

oxidizing conditions to form disulfide bonds in its protein coat.

Raising cortisol and depleting glutathione both tend to suppress the

cell-mediated immune response, which is needed to combat viral infections.

There also seems to be information suggesting that raising cortisol stimulates

the virus.

So it would seem that all of this would fit together well, and it would also

agree with the histories of many PWCs, who report that they experienced severe

stress of one kind or another before the onset of their illness. There has to be

a way to bring together these various histories with the common factor of the

presence of XMRV infection, and I think this model does that.

Rich