dc.creator | Tziastoudi M., Cholevas C., Stefanidis I., Theoharides T.C. | en |
dc.date.accessioned | 2023-01-31T10:21:31Z | |
dc.date.available | 2023-01-31T10:21:31Z | |
dc.date.issued | 2022 | |
dc.identifier | 10.1002/acn3.51631 | |
dc.identifier.issn | 23289503 | |
dc.identifier.uri | http://hdl.handle.net/11615/80238 | |
dc.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. © 2022 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association. | en |
dc.language.iso | en | en |
dc.source | Annals of Clinical and Translational Neurology | en |
dc.source.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85139381492&doi=10.1002%2facn3.51631&partnerID=40&md5=6fe9887aa21c2edd4527bbb7b5c7b35c | |
dc.subject | angiotensin converting enzyme 2 | en |
dc.subject | biological marker | en |
dc.subject | chemokine | en |
dc.subject | chemokine receptor CCR9 | en |
dc.subject | chemokine receptor CXCR6 | en |
dc.subject | chymase | en |
dc.subject | flavonoid | en |
dc.subject | HLA A antigen | en |
dc.subject | HLA C antigen | en |
dc.subject | HLA DQA1 antigen | en |
dc.subject | HLA DQB1 antigen | en |
dc.subject | HLA DRB1 antigen | en |
dc.subject | interleukin 1 | en |
dc.subject | luteolin | en |
dc.subject | toll like receptor | en |
dc.subject | toll like receptor 3 | en |
dc.subject | toll like receptor 7 | en |
dc.subject | vitamin D | en |
dc.subject | vitamin D binding protein | en |
dc.subject | vitamin D receptor | en |
dc.subject | allele | en |
dc.subject | Alzheimer disease | en |
dc.subject | biological phenomena and functions concerning the entire organism | en |
dc.subject | blood group ABO system | en |
dc.subject | blood group O | en |
dc.subject | cell activation | en |
dc.subject | chronic fatigue syndrome | en |
dc.subject | coronavirus disease 2019 | en |
dc.subject | cytokine signaling | en |
dc.subject | DNA polymorphism | en |
dc.subject | fatigue | en |
dc.subject | gene expression | en |
dc.subject | gene ontology | en |
dc.subject | genetic association | en |
dc.subject | genetic variability | en |
dc.subject | genome-wide association study | en |
dc.subject | genotype | en |
dc.subject | haplotype | en |
dc.subject | human | en |
dc.subject | immune response | en |
dc.subject | immune system | en |
dc.subject | immunopathology | en |
dc.subject | inflammation | en |
dc.subject | innate immunity | en |
dc.subject | mast cell | en |
dc.subject | microglia | en |
dc.subject | pathway analysis | en |
dc.subject | prevalence | en |
dc.subject | protein analysis | en |
dc.subject | respiratory failure | en |
dc.subject | Review | en |
dc.subject | risk factor | en |
dc.subject | signal transduction | en |
dc.subject | systematic review | en |
dc.subject | T lymphocyte activation | en |
dc.subject | whole exome sequencing | en |
dc.subject | cohort analysis | en |
dc.subject | genetics | en |
dc.subject | metabolism | en |
dc.subject | Cohort Studies | en |
dc.subject | COVID-19 | en |
dc.subject | Fatigue Syndrome, Chronic | en |
dc.subject | Humans | en |
dc.subject | Inflammation | en |
dc.subject | John Wiley and Sons Inc | en |
dc.title | Genetics of COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review | en |
dc.type | other | en |