Gemini
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@Jesse2233 many theories from your 50,000 foot overview are aggregated in the Solve ME/CFS 2017 Ramsay Award to the Bergquist et al team:
Our working hypothesis of ME/CFS pathogenesis is that a person predisposed for ME through genetics and previous antigen exposure is infected with a microbe prone to elicit ME. These microbial antigens have epitopes which cross-react with self-epitopes. An (auto)immune response to this microbe which bypasses tolerance mechanisms is elicited.
The cross-reactive immune response, e.g. autoantibodies, is directed against molecules involved in energy metabolism, hormonal regulation and, possibly, specific portions of the brain.
In short, “infection elicited autoimmunometabolic dysfunction”.
The role of infection may either be a “hit and run” phenomenon, or a chronic infection (“stay and fight”).
EDIT: Link-- http://solvecfs.org/2017-ramsay-award-program-team-1
Our working hypothesis of ME/CFS pathogenesis is that a person predisposed for ME through genetics and previous antigen exposure is infected with a microbe prone to elicit ME. These microbial antigens have epitopes which cross-react with self-epitopes. An (auto)immune response to this microbe which bypasses tolerance mechanisms is elicited.
The cross-reactive immune response, e.g. autoantibodies, is directed against molecules involved in energy metabolism, hormonal regulation and, possibly, specific portions of the brain.
In short, “infection elicited autoimmunometabolic dysfunction”.
The role of infection may either be a “hit and run” phenomenon, or a chronic infection (“stay and fight”).
EDIT: Link-- http://solvecfs.org/2017-ramsay-award-program-team-1
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