Seneca Valley virus 3C Protease Blocks EphA2-Mediated mTOR Activation to Facilitate Viral Replication.
3C protease (3C(pro))
Eph receptor A2 (EphA2)
Seneca Valley virus (SVV)
mTOR pathway
proteolysis
Journal
Microbial pathogenesis
ISSN: 1096-1208
Titre abrégé: Microb Pathog
Pays: England
ID NLM: 8606191
Informations de publication
Date de publication:
03 May 2024
03 May 2024
Historique:
received:
02
04
2024
revised:
24
04
2024
accepted:
01
05
2024
medline:
6
5
2024
pubmed:
6
5
2024
entrez:
5
5
2024
Statut:
aheadofprint
Résumé
The Seneca Valley virus (SVV) is a recently discovered porcine pathogen that causes vesicular diseases and poses a significant threat to the pig industry worldwide. Erythropoietin-producing hepatoma receptor A2 (EphA2) is involved in the activation of the AKT/mTOR signaling pathway, which is involved in autophagy. However, the regulatory relationship between SVV and EphA2 remains unclear. In this study, we demonstrated that EphA2 is proteolysed in SVV-infected BHK-21 and PK-15 cells. Overexpression of EphA2 significantly inhibited SVV replication, as evidenced by decreased viral protein expression, viral titers, and viral load, suggesting an antiviral function of EphA2. Subsequently, viral proteins involved in the proteolysis of EphA2 were screened, and the SVV 3C protease (3C
Identifiants
pubmed: 38705218
pii: S0882-4010(24)00140-2
doi: 10.1016/j.micpath.2024.106673
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
106673Informations de copyright
Copyright © 2024. Published by Elsevier Ltd.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare no conflict of interest.