Synergetic contributions of Seneca Valley virus 3 C and 3D proteins to induction of ferroptosis for viral replication.

ABSTRACT: Seneca Valley virus (SVV) infection leads to severe vesicular diseases in pigs, posing a significant threat to the global swine industry. Ferroptosis, a novel form of non-apoptotic cell death, is characterized by iron-dependent phospholipid peroxidation. However, the role of ferroptosis in SVV replication remains poorly understood. In this study, we demonstrate that SVV infection induces ferroptosis, as evidenced by lipid peroxidation, reactive oxygen species (ROS) accumulation, and glutathione (GSH) depletion. The GPX4 and nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy are key contributors to ferroptosis induction. Furthermore, our findings reveal that the SVV 3 C proteinase (3C^pro) targets the GPX4 for degradation, thereby promoting ferroptosis. Simultaneously,

SUBMITTER: Song J 

PROVIDER: S-EPMC12618751 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature