Thanks for posting
@osisposis. I used to think our problem was chronic infection (perhaps especially EBV), but now I'm not convinced. I think a huge problem with the evidence cited in this article is that what they generally measure is not the infection itself, but the immune system's response to it. So for example, we all could have normal viral loads for many of these viruses, but be overproducing antibodies etc. to them. On most of the tests, you can't tell the difference between these two possibilities.
I'm thinking now that our problem is less likely to be ongoing infection, and more likely to be some ongoing weirdness in our immune response. There were a few things that tipped the balanced for me. One was how diverse everyone's initial infections were - even if you just look at people whose illness started with an acute viral illness. It seems many roads can lead to the same outcome.
Another thing for me was the tales from responders to rituximab. If the problem were something like viral load (perhaps EBV infecting the B cells), then removing a large portion of the infected cells should lead to a lasting recovery. But even in ritux responders, the recovery is short-lived. Once a new panel of B cells is produced, the problem returns. If the problem were chronic viral infection, why would it come back so readily after wiping out such a large number of the infected host cells? Okay, so maybe whatever infected host cells remained were able to gain a foothold and proliferate. But then you have to explain why this doesn't happen in "normal" people, who also carry EBV infected B cells. How come the virus doesn't gain a foothold in them? t all boils down to some abnormality in our immune system.
But maybe someone who's more expert can comment?
