Porcine reproductive and respiratory syndrome virus infection induces endoplasmic reticulum stress, facilitates virus replication, and contributes to autophagy and apoptosis.

ABSTRACT: During viral infection, the host cell synthesizes high amounts of viral proteins, which often causes stress to the endoplasmic reticulum (ER). To manage abnormal ER stress, mammalian cells trigger a response called the unfolded protein response (UPR). Previous studies have indicated that porcine reproductive and respiratory syndrome virus (PRRSV), an Arterivirus that has been devastating the swine industry worldwide, can induce ER stress and activate UPR, however, the activation pathways and the biological significance requires further investigation. In this study, we demonstrated that, among the three types of UPR pathways, PRRSV infection induced PERK and IRE1 pathways, but not the ATF6 pathway. Furthermore, the induction of UPR promoted PRRSV replication. We also found that PRRSV-induce

SUBMITTER: Chen Q 

PROVIDER: S-EPMC7403369 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature