The relationship between autophagy and apoptosis during pseudorabies virus infection

Abstract

Both autophagy and apoptosis are mechanisms that maintain homeostasis in cells and that play essential roles in viral infections. Previous studies have demonstrated that autophagy and apoptosis pathways occurred with complex relationships in virus-infected cells. However, the regulation between these two processes in Pseudorabies virus (PRV) infection remains unclear. In the present study, we demonstrated that activated autophagy was induced at the early stage of PRV infection and that apoptosis was induced at the late stage of infection. Autophagy induction inhibited apoptosis and decreased viral replication, and autophagy inhibition promoted apoptosis and increased viral replication. We also found that viral infection resulted in an increase in the production of reactive oxygen species (ROS) and activation of apoptosis in autophagy-impaired cells, suggesting that ROS may participate in the cross-talk between autophagy and apoptosis in PRV-infected cells. Our studies provide possible molecular mechanisms for the cross-talk between apoptosis and autophagy induced by PRV infection in porcine cells. This suggests that these two cell death processes should be considered as the same continuum rather than as completely separate processes.

Pseudorabies virus causes splenic injury via inducing the oxidative stress and apoptpsos related factors in mice

“…Generally, apoptosis is activated mainly in the late stage of infection by PRV. Moreover, studies have shown that PRV triggers ROS production and causing of apoptosis in autophagic-damaged cells, which indicated that ROS may be participated in the linking of autophagy and apoptosis in cells infected by PRV [15]. Oxidative stress is associated with various cell death processes, including apoptosis, caused by viral infection.…”