Major vault protein inhibits CSFV replication by promoting cell apoptosis.

Abstract

Classical swine fever virus (CSFV) remains a major pathogen posing substantial threats to the global swine industry. CSFV infection modulates the expression of numerous host cell proteins, with certain factors facilitating viral replication while others exert inhibitory effects. This study investigated the influence of CSFV infection on Major Vault Protein (MVP) expression, revealing that CSFV upregulates MVP in PK-15 cells. Functional analyses demonstrated that stable MVP overexpression significantly suppressed CSFV replication, whereas MVP knockout enhanced viral propagation. Furthermore, MVP was found to upregulate pro-apoptotic proteins Bax, caspase-3, and caspase-9-while downregulating the anti-apoptotic protein Bcl-2. These results indicate that MVP promotes apoptosis and that MVP-mediated apoptotic mechanisms contribute to the inhibition of CSFV replication. Collectively, these findings suggest that CSFV-induced MVP upregulation promotes apoptosis, thereby restricting viral replication. MVP may therefore represent a promising molecular target for developing novel therapeutic interventions against CSFV infection.