I'll write an answer to that in the upcoming weeks. I believe that I can give you very good arguments on all of the questions you raise that do make HHV-6b reactivation hypothesis the most plausible of all the ideas on causative mechanism that were brought forward.OK, but why pick HHV-6B reactivation? There may be some data on increased levels in saliva but how does HHV-6 explain things any better than anything else? And why is it reactivated (which would be the real question) and how would explain delayed PEM?
You seem to be starting from the assumption that HHV6 has the edge on other things but I suspect other members here haven't heard a reason for it.