Later work by those scientists showed that the same viruses are present in healthy people:
The fact that the same non-cytolytic enterovirus infection is also found in the muscles of healthy people was known even in their earliest work. But the prevalence of these muscle infections was much higher in ME/CFS patients.
That's normally what you demonstrate in pathogen studies: you show that the pathogen is much more prevalent in the disease patients than in the healthy controls. In that way, you prove an association. Of course proving whether or not the pathogen actually causes the disease requires more research.
But there is nothing in the enterovirus muscle infection research that disproves the possibility that this virus may cause ME/CFS.
There is also the enterovirus brain infection research, which so far shows complete 100% correlation between the presence of the infection and ME/CFS.
That's not quite true. Cortisol doesn't turn down the immune system, it shifts it from Th1 (intracellular) to Th2 (extracellular) response.
You are right, it's just the Th1 response cortisol reduces, which results in a Th2 boost.
The results were not statistically significant.
The study's conclusion that responders were 7.4 times more likely to be in the Valcyte group was a statistically significant finding (p-value = 0.029).
But the limitations of the Montoya study were the small amount of patients, and the very short treatment time of only 6 months. Lerner's study indicates that improvement is gradual, and takes 3 months for the benefits to begin to appear, and around 2 years for the full benefits to manifest, with not much further improvement being made after the 2 year point.
You can see the gradual improvements in Table 3 of Lerner's study, which I copied into
this post.
It could also have been that the treatment had no effect, and both groups gradually improved but the more ill group just took longer to improve.
That's a possibility, but if you look at studies which have examined the improvement and recovery rate of ME/CFS patients, in the general case they show that improvement and recovery is rare (see
this study which found improvement in less than 6% of patients after 5 years).
So the improvements in Lerner's patients seem unlikely to be due to natural improvement, because it seems there is rarely natural improvement in ME/CFS in general.
However, for the post mononucleosis ME/CFS subset, recovery looks
much more common:
this study found that at first contact, 10% of patients were still working, but after 7 years, 55% were at work.
So post-mono ME/CFS seems to have a far more optimistic prognosis than ME/CFS in the general case (ME/CFS linked to other viral or non-triggers).
Maybe EBV-linked ME/CFS is just "ME/CFS lite" compared to the ME/CFS associated with other viruses?