Rab11a is required for porcine reproductive and respiratory syndrome virus induced autophagy to promote viral replication.

Porcine reproductive and respiratory syndrome virus (PRRSV) is the leading virus known to cause massive economic loss in pig industry worldwide. In our previous study, transcriptional profiling of PRRSV-infected lung tissue of Tongcheng and Landrane pigs, which have highly pathogenic PRRSV (HP-PRRSV) susceptibility differences, showed differential expression of Rab11a. The small GTPase Rab11a regulates intracellular membrane trafficking events involved in autophagy. However, the involvement of the convergence of endosomal Rab11a and autophagy pathways during PRRSV infection is still unclear. In this study, we demonstrated that PRRSV infection induced complete autophagy and up-regulated the expression of Rab11a. Furthermore, interference of the expression of Rab11a resulted in the accumulation of endogenous LC3-II and p62, indicating that Rab11a played a vital role in autophagosome maturation. Silencing of Rab11a resulted in a compromise the expression of intracellular viral NSP2 and ORF7. Besides, confocal microscopy analysis showed that viral NSP2 was colocalized with Rab11a in Marc145 cells. Collectively, our findings revealed that Rab11a acted as a proviral host factor that benefited PRRSV replication in a manner that correlates with autophagy.