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

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...

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Autores principales: Tziastoudi, Maria, Cholevas, Christos, Stefanidis, Ioannis, Theoharides, Theoharis C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9639636/
https://www.ncbi.nlm.nih.gov/pubmed/36204816
http://dx.doi.org/10.1002/acn3.51631
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author Tziastoudi, Maria
Cholevas, Christos
Stefanidis, Ioannis
Theoharides, Theoharis C.
author_facet Tziastoudi, Maria
Cholevas, Christos
Stefanidis, Ioannis
Theoharides, Theoharis C.
author_sort Tziastoudi, Maria
collection PubMed
description 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 pubmed-96396362022-11-14 Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review Tziastoudi, Maria Cholevas, Christos Stefanidis, Ioannis Theoharides, Theoharis C. Ann Clin Transl Neurol Review Article 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. John Wiley and Sons Inc. 2022-10-06 /pmc/articles/PMC9639636/ /pubmed/36204816 http://dx.doi.org/10.1002/acn3.51631 Text en © 2022 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Review Article
Tziastoudi, Maria
Cholevas, Christos
Stefanidis, Ioannis
Theoharides, Theoharis C.
Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review
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
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9639636/
https://www.ncbi.nlm.nih.gov/pubmed/36204816
http://dx.doi.org/10.1002/acn3.51631
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