Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review

Abstract

COVID‐19 and ME/CFS present with some similar symptoms, especially physical and mental fatigue. In order to understand the basis of these similarities and the possibility of underlying common genetic components, we performed a systematic review of all published genetic association and cohort studies regarding COVID‐19 and ME/CFS and extracted the genes along with the genetic variants investigated. We then performed gene ontology and pathway analysis of those genes that gave significant results in the individual studies to yield functional annotations of the studied genes using protein analysis through evolutionary relationships (PANTHER) VERSION 17.0 software. Finally, we identified the common genetic components of these two conditions. Seventy‐one studies for COVID‐19 and 26 studies for ME/CFS were included in the systematic review in which the expression of 97 genes for COVID‐19 and 429 genes for ME/CFS were significantly affected. We found that ACE, HLA‐A, HLA‐C, HLA‐DQA1, HLA‐DRB1, and TYK2 are the common genes that gave significant results. The findings of the pathway analysis highlight the contribution of inflammation mediated by chemokine and cytokine signaling pathways, and the T cell activation and Toll receptor signaling pathways. Protein class analysis revealed the contribution of defense/immunity proteins, as well as protein‐modifying enzymes. Our results suggest that the pathogenesis of both syndromes could involve some immune dysfunction.

Converging Evidence of Similar Symptomatology of ME/CFS and PASC Indicating Multisystemic Dyshomeostasis

“…It is speculated that the post-viral pathogenesis of PASC may be similar to, or even identical to, that of ME/CFS [1]. A number of researchers have proposed pathophysiological mechanisms that may account for the similarities between ME/CFS and PASC [1][2][3][4][5][6]. The aims of this article are: (i) to indicate the converging evidence that ME/CFS and PASC involve a highly similar constellation of symptoms; (ii) to propose the hypothesis that ME/CFS and PASC have a similar etiology founded on a breakdown of the body's central systems of homeostasis; and (iii) to indicate the possibility that neuroinflammation may be responsible for the dyshomeostasis that occurs in ME/CFS and PASC.…”