Genetics of COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review.
Tziastoudi, Maria, Cholevas, Christos, Stefanidis, Ioannis et al. · Annals of clinical and translational neurology · 2022 · DOI
Quick Summary
This study looked at genetic research on both COVID-19 and ME/CFS to see if they share common genetic factors that might explain why both conditions cause extreme fatigue. Researchers reviewed 71 studies on COVID-19 genetics and 26 studies on ME/CFS genetics, then identified six genes that appear in both conditions. The findings suggest that immune system dysfunction—specifically problems with inflammation and how immune cells communicate—may play a role in both illnesses.
Why It Matters
This research provides important evidence that ME/CFS and COVID-19 may share underlying genetic vulnerabilities related to immune dysfunction, which could help explain why some people develop ME/CFS after COVID-19 infection. Understanding these shared genetic pathways could inform future diagnostic approaches and therapeutic targets for both conditions. The identification of specific genes involved offers a foundation for more targeted research into the biological mechanisms of ME/CFS.
Observed Findings
Six genes (ACE, HLA-A, HLA-C, HLA-DQA1, HLA-DRB1, TYK2) showed significant genetic associations in both COVID-19 and ME/CFS studies.
Pathway analysis identified chemokine and cytokine signaling as commonly affected functional pathways in both conditions.
T cell activation and Toll-like receptor signaling pathways were highlighted as contributing to both syndromes.
Defense/immunity proteins and protein-modifying enzymes were identified as key protein classes involved.
97 genes showed significant expression changes in COVID-19 studies, while 429 genes were identified in ME/CFS studies.
Inferred Conclusions
Both COVID-19 and ME/CFS likely involve immune system dysfunction as a central pathogenic mechanism.
Shared genetic components suggest a biological basis for why some COVID-19 patients may develop ME/CFS-like symptoms or post-COVID conditions.
Immune dysregulation pathways, particularly those involving inflammation and T cell function, may be critical to understanding disease mechanisms in both conditions.
Genetic predisposition may influence susceptibility to these conditions, though environmental factors likely also play important roles.
Remaining Questions
What environmental triggers or additional factors determine whether genetically predisposed individuals actually develop ME/CFS or COVID-19?
What This Study Does Not Prove
This study does not prove that these genetic variants cause ME/CFS or COVID-19, only that they are statistically associated with these conditions. The findings are correlational and do not establish causation or explain why some genetically predisposed individuals develop these diseases while others do not. The review also cannot determine whether genetic factors alone are sufficient to cause disease or what environmental triggers may be necessary.