Figure 1.

Apoptosis, autophagy, and pyroptosis in the pathogenesis of classical swine fever virus (CSFV). CSFV and its coding protein E^rns trigger apoptosis. The apoptosis of immune cells is beneficial for CSFV to escape the monitoring of the host immune system. Importantly, the CSFV nonstructural proteins N^pro and NS2 inhibit apoptosis, which may be an important process for the virus to achieve persistent infection. CSFV infection induces autophagy and mitophagy and utilizes their mechanisms for viral replication and virion release. Moreover, CSFV-induced autophagy inhibits cell apoptosis by downregulating retinoic acid inducible gene-I (RIG-I)-like receptor (RLR) signaling-mediated levels of type I interferon production, which may be an important mechanism for the immune escape of CSFV. CSFV infection promotes the activation of NLRP3 inflammasome-mediated pyroptosis, which may help explain why CSFV establishes a persistent infection in leukocytes.