Pseudorabies virus induces autophagy to enhance viral replication in mouse neuro-2a cells in vitro.

Autophagy of cytoplasmic components plays an essential role in the pathogenic infection process. Furthermore, research suggests that autophagy is an extremely important component of the innate immune response. Our study aimed to reveal the effect of virus-induced autophagy on pseudorabies virus (PRV) replication. Our results confirmed that light chain 3 (LC3)-I was converted into LC3-II after PRV infection; this transition is considered an important indicator of autophagy. Transmission electron microscopy (TEM) revealed that PRV infection could notably increase the number of autophagosomes in mouse neuro-2a (N2a) cells. In addition, LC3-II accumulated in response to chloroquine (CQ) treatment, indicating that PRV infection induced a complete autophagic flux response. Furthermore, our analyses verified differences in the magnitude of autophagy induction by two different PRV isolates, LA and ZJ01. Subsequent analysis showed that the induction of autophagy by rapamycin facilitated PRV replication, while inhibition of autophagy by 3-methyladenine (3-MA) reduced PRV replication. These results indicated that PRV induced autophagy via the classical Beclin-1-Atg7-Atg5 pathway to enhance viral replication in N2a cells in vitro.