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 cohor...

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Main Authors: Maria Tziastoudi, Christos Cholevas, Ioannis Stefanidis, Theoharis C. Theoharides
Format: Article
Language:English
Published: Wiley 2022-11-01
Series:Annals of Clinical and Translational Neurology
Online Access:https://doi.org/10.1002/acn3.51631
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author Maria Tziastoudi
Christos Cholevas
Ioannis Stefanidis
Theoharis C. Theoharides
author_facet Maria Tziastoudi
Christos Cholevas
Ioannis Stefanidis
Theoharis C. Theoharides
author_sort Maria Tziastoudi
collection DOAJ
description 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.
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spelling doaj.art-f09441ce8a6a49de91c9f157eed4ef172022-12-22T04:11:40ZengWileyAnnals of Clinical and Translational Neurology2328-95032022-11-019111838185710.1002/acn3.51631Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic reviewMaria Tziastoudi0Christos Cholevas1Ioannis Stefanidis2Theoharis C. Theoharides3Department of Nephrology, Faculty of Medicine, School of Health Sciences University of Thessaly Larissa GreeceFirst Department of Ophthalmology, Faculty of Health Sciences Aristotle University, AHEPA Hospital Thessaloniki GreeceDepartment of Nephrology, Faculty of Medicine, School of Health Sciences University of Thessaly Larissa GreeceInstitute of Neuro-Immune Medicine Nova Southeastern University Clearwater FL USAAbstract 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.https://doi.org/10.1002/acn3.51631
spellingShingle Maria Tziastoudi
Christos Cholevas
Ioannis Stefanidis
Theoharis C. Theoharides
Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review
Annals of Clinical and Translational Neurology
title Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review
title_full Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review
title_fullStr Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review
title_full_unstemmed Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review
title_short Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review
title_sort genetics of covid 19 and myalgic encephalomyelitis chronic fatigue syndrome a systematic review
url https://doi.org/10.1002/acn3.51631
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AT ioannisstefanidis geneticsofcovid19andmyalgicencephalomyelitischronicfatiguesyndromeasystematicreview
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