To me, 6 of 11 (meaning 5 didn't respond to the treatment) doesn't strongly support the hypothesis. It tells me that the hypothesis only applies to a limited subset of ME/CFS, and thus isn't the core cause.
I am not sure that conclusion necessarily follows, as in the non-responders to interferon, their ME/CFS might conceivably still be due to enterovirus, but they just did not respond to the anti-enteroviral treatment. There are few medical treatments that work universally on all patients. Whether it works or not often comes down to individual genetics.
The same is true in the interferon treatment of hepatitis C virus: this only works on a subset, but nobody would suggest that the patients it fails to work on do not have hep C, or that their symptoms are not caused by this hep C virus. In hepatitis C virus infection the genetics behind the response to interferon have been studied.
Furthermore, if it was only tested on a limited subset (those who were severely bedbound), did the researchers expect that it wouldn't work on non-bed-bound victims?
I don't think so, because apart from Dr Chia's interferon study, two previous interferon studies also showed this treatment works on enterovirus ME/CFS patients, and I don't think these other studies only focused on severe patients.
To me the hypothesis should be: 'Chronic viral infection may cause ME/CFS victims to experience more severe symptoms than those without such infection'. The results support that hypothesis.
That hypothesis would make sense if patients already had some degree of fatigue and brain fog before they caught the viral infection which triggered their ME/CFS, and the viral infection then just worsened their symptoms. But people are normally completely without any ME/CFS symptoms before their viral infection, and then they develop full ME/CFS afterwards. So to me that does not suggest the viral infection worsens ME/CFS, but suggests it may be the cause of it.
But certainly some infections can be exacerbating factors in ME/CFS, like Bartonella, Babesia or Brucella.
The trouble with interferon treatment of enterovirus is that unlike with hepatitis C virus, it does not fully eliminate the enterovirus from the body. So the virus is still there, and that may explain why the patients were not fully free of ME/CFS symptoms after in treatment; and it most likely explains why their ME/CFS returns a few months post-treatment, as the virus slowly grows back.
If drug companies were to develop a drug that could fully eliminate enterovirus, then we could very easily work out whether enterovirus is the sole cause of ME/CFS in the enterovirus subset.
By the way, I've just written an MEpedia article on
non-cytolytic / non-cytopathic enterovirus, which is the particular mutated form of enterovirus found in ME/CFS. This mutated enterovirus follows a different lifecycle compared to regular enterovirus, which is why it is so hard to eliminate.