SK2018
SK
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Dysfunctional B cells autoreacting to unknown self antigens most likely.
That would explain the relapse after RTX ,.memory B cells return as obviously the naive cells are still making the same mistake upon re maturing.
That would explain the relapse after RTX ,.memory B cells return as obviously the naive cells are still making the same mistake upon re maturing.
@Hip, that was pretty much my working theory for ages, but now I'm not so sure. This is a repeat of stuff I said not long ago, but the things that made me doubt the B-cell infection hypothesis were:
* The absence of MECFS symptoms in HIV+ people, despite proliferation of herpes viruses. They even get cancers that are directly associated with herpes viruses, like karposy's sarcoma. But even so, its not till the very late stages that HIV+ people feel really fatigued and sick, well after the herpes proliferation has begun to happen. They don't have the feeling ill part - which suggests to me there's something more to MECFS.
* The short lived effects of rituximab on MECFS symptoms. If the problem were viral load alone, removal of a good portion of the infected cells should alleviate the problem for good. You'd have no greater viral load than any normal healthy person (who almost all harbour latent herpes viruses). But it turns out rtx only gives temporary relief; the symptoms soon return. You might say "well, that's because there were still enough infected cells to restart the infection". But then normal people carry some herpes infected cells too, why doesn't it take root in them? Again, the answer seems to be there is something different going on with us, that can't be explained by viral load alone.
* The mutliple triggers for MECFS. The Dubbo studies showed a good proportion of people with certain non-herpes infections end up with MECFS too. Ross River virus and Q fever have nothing to do with herpes, yet they can give rise to a chronic condition that looks identical to the ones seen following an acute EBV infection. Okay, so maybe you could say that the initial infection provides the opportunity for the herpes virus to reproduce, by stimulating replication of the infected B cells. But it could easily be something more generic - stimulating the immune system in some way.
Maybe herpes has a role to play in creating the conditions that make our immune systems spiral out of control. But perhaps its just too simple to say MECFS is just a problem with high levels of latent herpes infection.