Seneca Valley virus induces mitochondrial apoptosis by activating ER stress or the PERK pathway based on Ca²⁺ transfer from ER to mitochondria.

ABSTRACT: Seneca Valley virus (SVV), also known as Senecavirus A, a porcine pathogen that causes vesicular diseases, is prevalent in pig herds worldwide. SVV infection induces endoplasmic reticulum (ER) stress in PK-15 and BHK-21 cells, accompanied by activation of the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) and activating transcription factor 6 (ATF6) pathways, which in turn facilitates SVV replication. ER stress is associated with the regulation of Ca²⁺ homeostasis and mitochondrial apoptosis. However, the precise role of Ca²⁺ in SVV-induced apoptosis remains unclear. In this study, western blotting, flow cytometry, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) detection revealed that either ER stress or the P

SUBMITTER: Hou L 

PROVIDER: S-EPMC11915807 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature