Genetics of COVID-19 and ME/CFS: a systematic review
Greek researchers found 71 studies for COVID-19 and 26 studies for ME/CFS that looked at genes. They concluded:
Venn diagram regarding the significant genes of COVID-19 and ME/CFS.
“In spite of the fact that COVID-19 and ME/CFS present with some similar symptoms, especially physical and mental fatigue, genetic association, and cohort studies indicate that these two complex diseases share only a few common genes. These… appear to be involved in the regulation of immune processes.
This finding supports the notion that the pathogenesis of both syndromes may derive from some aberrant and lasting immune response, possibly involving mast cells and microglia, which have been recently implicated in both diseases.
Understanding the basis of this immune dysfunction could help with the diagnosis, prognosis, and treatment of these debilitating conditions.
Genetics of COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review, by Maria Tziastoudi, Christos Cholevas, Ioannis Stefanidis, Theoharis C Theoharides in Ann Clin Transl Neurol. 2022 Oct 6 [doi: 10.1002/acn3.51631]
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.
