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Variants (below) in the complement pathway increase susceptibility to ME/CFS, and patients with ME/CFS are about twice as likely to have mannose-binding lectin deficiency, which increases susceptibility to fungal and viral infections.[ref] IDO trap: IDO2 gene One theory of ME/CFS is that there is a metabolic trap in the tryptophan pathway that shifts the way tryptophan is metabolized
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The metabolic syndrome can directly influence OA development by promoting the generation of pro-inflammatory and catabolic factors, as well as indirectly by interfering with autophagy and senescence (28)
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