The complex interplay between encephalomyocarditis virus and the host defence system.
Encephalomyocarditis virus
apoptosis
autophagy
inflammatory responses
innate immune response
type I IFN
Journal
Virulence
ISSN: 2150-5608
Titre abrégé: Virulence
Pays: United States
ID NLM: 101531386
Informations de publication
Date de publication:
Dec 2024
Dec 2024
Historique:
medline:
28
7
2024
pubmed:
28
7
2024
entrez:
27
7
2024
Statut:
ppublish
Résumé
A variety of animals can be infected by encephalomyocarditis virus (EMCV). EMCV is the established causative agent of myocarditis and encephalitis in some animals. EMCV causes high fatality in suckling and weaning piglets, making pigs the most susceptible domestic animal species. Importantly, EMCV has zoonotic potential to infect the human population. The ability of the pathogen to avoid and undermine the initial defence mechanism of the host contributes to its virulence and pathogenicity. A large body of literature highlights the intricate strategies employed by EMCV to escape the innate immune machinery to suit its "pathogenic needs." Here, we also provide examples on how EMCV interacts with certain host proteins to dampen the infection process. Hence, this concise review aims to summarize these findings in a compendium of decades of research on this exciting yet underappreciated topic.
Identifiants
pubmed: 39066684
doi: 10.1080/21505594.2024.2383559
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM