alex3619
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Waverunner, but there is a flip side to this argument. What if its both environment and what we call the trigger? In other words, a confluence of events. Not everyone will experience the same environmental impact, not everyone has the same genes, not everyone has any particular pathogen attack and persist the same way. What if its a combination of these factors? Also there is the issue of viral life cycles. Even when I was learning biochemistry up to 2002, it was presumed that the virus life cycle consisted of the lytic cycle: replicate, lyse the cell, spread, infect new cell, repeat. Now we know thats one of at least several lifecycles, and that "latent" viruses can be quite active.
Don't forget that if environmental factors are ruled out because not everyone with those factors has ME or CFS, then so are all the pathogens. Not everyone with any of these pathogens has ME or CFS. There is perhaps one caveat to that: most CFS patients (not defined as ME I think, but I could be wrong) have enterviral infections that are "latent", which really means they are following one of the other two lifecycles. This is the same virus family as polio, and I suspect its not a coincidence that ME used to be called atypical polio.
Don't forget that if environmental factors are ruled out because not everyone with those factors has ME or CFS, then so are all the pathogens. Not everyone with any of these pathogens has ME or CFS. There is perhaps one caveat to that: most CFS patients (not defined as ME I think, but I could be wrong) have enterviral infections that are "latent", which really means they are following one of the other two lifecycles. This is the same virus family as polio, and I suspect its not a coincidence that ME used to be called atypical polio.