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  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
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Genetics of COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review

Thumbnail
Auteur
Tziastoudi M., Cholevas C., Stefanidis I., Theoharides T.C.
Date
2022
Language
en
DOI
10.1002/acn3.51631
Sujet
angiotensin converting enzyme 2
biological marker
chemokine
chemokine receptor CCR9
chemokine receptor CXCR6
chymase
flavonoid
HLA A antigen
HLA C antigen
HLA DQA1 antigen
HLA DQB1 antigen
HLA DRB1 antigen
interleukin 1
luteolin
toll like receptor
toll like receptor 3
toll like receptor 7
vitamin D
vitamin D binding protein
vitamin D receptor
allele
Alzheimer disease
biological phenomena and functions concerning the entire organism
blood group ABO system
blood group O
cell activation
chronic fatigue syndrome
coronavirus disease 2019
cytokine signaling
DNA polymorphism
fatigue
gene expression
gene ontology
genetic association
genetic variability
genome-wide association study
genotype
haplotype
human
immune response
immune system
immunopathology
inflammation
innate immunity
mast cell
microglia
pathway analysis
prevalence
protein analysis
respiratory failure
Review
risk factor
signal transduction
systematic review
T lymphocyte activation
whole exome sequencing
cohort analysis
genetics
metabolism
Cohort Studies
COVID-19
Fatigue Syndrome, Chronic
Humans
Inflammation
John Wiley and Sons Inc
Afficher la notice complète
Résumé
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.
URI
http://hdl.handle.net/11615/80238
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  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [19735]

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