Thinking about this study a bit more:
The authors found a twofold increase in the risk of developing ME/CFS in those who were diagnosed with H1N1 swine flu. I assume this increase in risk is relative to the general population (who were not diagnosed with H1N1 influenza).
But note that the number of people who caught the H1N1 virus will be higher than the number of people actually diagnosed with having H1N1 influenza (because the majority of people catching the virus would have only had minor symptoms, or have been asymptomatic, so were not diagnosed).
Studies show that just after the 2009 pandemic, around 24% of the general population, and 50% of school-age children were seropositive for H1N1, meaning they had caught the virus at some point.
So, people actually diagnosed with H1N1 influenza in general must have been hit much harder by the H1N1 virus, because presumably these were the people whose symptoms were so bad on contracting H1N1 that they had to go to their doctor.
Thus what this study may be measuring is
how severely someone's body or immune system may be reacting to the H1N1 virus. By focusing on those who were actually diagnosed with H1N1 influenza, rather than focusing on the larger set of people those who are seropositive for H1N1, this study may merely be selecting people whose immune system reacts more strongly to a H1N1 viral infection.
Now people who naturally mount a strong inflammatory response to viral infection might conceivably be much more likely to develop ME/CFS, given that ME/CFS is often viewed as a chronic inflammatory condition driven by viral infection. So this might explain why people from the group diagnosed with H1N1 influenza were found to be at higher risk for later developing ME/CFS.
Thus I can see two ways we can interpret the results of this study:
(1) The first interpretation is that
H1N1 influenza virus does not trigger ME/CFS, but those who get major influenza symptoms on catching from H1N1 may simply be more immunologically disposed to developing ME/CFS (but only when they catch the usual ME/CFS-triggering viruses like enterovirus or EBV).
(2) The second interpretation is that
H1N1 influenza virus does sometimes trigger ME/CFS.
Possibly one way to work out when the first or second interpretation might be correct is to look at the timing of the onset of ME/CFS after coming down with H1N1 influenza. We know with the usual ME/CFS-triggering viruses, you tend to get either rapid-onset ME/CFS (the disease appearing within days of contracting the triggering virus), or you get gradual-onset ME/CFS (the disease appearing within a few months of contracting the triggering virus).
So if we looked at the average time of onset of ME/CFS during the 39 months that the cohort was tracked, if there are a lot of cases of ME/CFS appearing withins days of coming down with their H1N1 influenza, or within a few months of their H1N1 influenza, then that suggests the H1N1 virus is actually
triggering ME/CFS.
But if the typical onset time of ME/CFS is found at random times during the 39 month observation period, that suggests the H1N1 virus
is not triggering ME/CFS.
Perhaps we will find some info on the onset time of ME/CFS in the full paper.
There is also a third possibility:
(3) The third interpretation is that H1N1 influenza virus does not
trigger ME/CFS as such, but after coming down with a major case of H1N1 influenza, the body becomes more vulnerable to later developing ME/CFS (when catching one of the usual ME/CFS triggering viruses like enterovirus or EBV).