With localized ME/CFS outbreaks such as the Royal Free Hospital outbreak, or the Lake Tahoe outbreak, you have to explain two things: why the virus causes such a very high incidence of ME/CFS in the locale, but then causes very little further problems as the virus spreads to people outside of that locale.
The only logical explanation I can see is a
dual causal factor theory of ME/CFS, with this disease being triggered by an ME/CFS-associated virus
in combination with another pernicious factor that is only present in that locale. That explains why the rate of ME/CFS is so high in the locale, but as the virus spreads outside the locale, it produces very little new cases of ME/CFS.
If you consider the Lake Tahoe outbreak, we know that during the outbreak, there was a large toxic algae bloom on the lake (and biotoxins such as toxic algae or mold can cause disease just on their own — Dr Shoemaker's CIRS illness is due to these biotoxins). There was also some known issues of mold problems in certain municipal building in the Lake Tahoe area.
In the Royal Free Hospital, we don't have any information about any possible biotoxins or other localized pernicious factors; but my personal theory is that there may have been water damage and a toxic mold growth in communal staff rooms or staff canteens in one or more of the hospital buildings, which in combination with the virus, caused the Royal Free outbreak. This theory would also explain why it was only the staff, but not the hospital patients, who were hit with the ME/CFS (because only the staff would go into the mold-infested staff rooms or staff canteens).
I posted some info about this dual causal factor theory of ME/CFS during outbreaks in
this post.
One fact that tends to corroborate this dual causal factor theory is Dr John Chia's discovery that an acute viral infection + corticosteroids often causes ME/CFS (see
this thread). Dr Chia investigated thousands of ME/CFS patients' case histories, and noted that ME/CFS was often triggered in these patients when corticosteroids were prescribed during the course of an acute infection. Corticosteroids weaken the immune response, so it seem that when the immune response is weakened during the time of an acute infection when you first catch a virus linked to ME/CFS, that creates the conditions necessary for the virus to trigger ME/CFS.
So with acute viral infection + corticosteroids, we see another example of the dual causal factor theory of ME/CFS.
I think to toxic algae or mold may have analogous immunosuppressive effects to corticosteroids, weakening the immune response in such a way that allows the virus to trigger ME/CFS.