Mitochondria-mediated oxidative stress during viral infection.
antioxidant therapy
electron transport chain (ETC)
endoplasmic reticulum (ER) stress
intrinsic apoptosis
oxidative phosphorylation (OXPHOS)
reactive oxygen species (ROS)
Journal
Trends in microbiology
ISSN: 1878-4380
Titre abrégé: Trends Microbiol
Pays: England
ID NLM: 9310916
Informations de publication
Date de publication:
07 2022
07 2022
Historique:
received:
20
06
2021
revised:
20
12
2021
accepted:
21
12
2021
pubmed:
23
1
2022
medline:
18
6
2022
entrez:
22
1
2022
Statut:
ppublish
Résumé
Through oxidative phosphorylation, mitochondria play a central role in energy production and are an important production source of reactive oxygen species (ROS). Not surprisingly, viruses have evolved to exploit this organelle in order to support their infection cycle. Beyond its role in the cellular antiviral response, induction of oxidative stress has emerged as a common strategy employed by many viruses to promote their replication. Here, we review the key molecular mechanisms employed by viruses to interact with mitochondria and induce oxidative stress. Furthermore, we discuss how viruses benefit from increased ROS levels, how they control ROS production to maintain a favorable redox environment, and how they cope with ROS-mediated cell death.
Identifiants
pubmed: 35063304
pii: S0966-842X(21)00318-8
doi: 10.1016/j.tim.2021.12.011
pii:
doi:
Substances chimiques
Reactive Oxygen Species
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
679-692Informations de copyright
Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.