LiyanCao,  MeiXue,  JianfeiChen,  HongyanShi,  XinZhang,  DaShi,  JianboLiu,  LipingHuang,  YanwuWei,  ChangmingLiu,  LiFeng

Virology. 2019 Sep 26;539:1-10. doi: 10.1016/j.virol.2019.09.012

Abstract

Endoplasmic reticulum (ER) stress is associated with numerous mammalian diseases, especially viral diseases. Porcine parvovirus (PPV) is the causative agent of reproductive failure in swine. Here, we observed that the PPV infection of porcine kidney 15 and porcine testis cells resulted in the activation of ER stress sensors mediated by protein kinase R-like ER kinase (PERK), but not inositol-requiring enzyme 1 and activating transcription factor 6 (ATF6). ER stress activation obviously blocked PPV replication. Depletion of proteins, such as PERK, eukaryotic initiation factor 2, and ATF4, by small interfering RNA significantly enhanced PPV replication. Moreover, the pro-apoptotic factor C/EBP homologous protein was identified a key factor in the inhibition of PPV replication. These data demonstrate that PPV infection activates ER stress through the PERK signaling pathway and that ER stress inhibits further PPV replication by promoting apoptosis.

Copyright © 2019 Elsevier Inc. All rights reserved.

KEYWORDS:

Apoptotic cell death; Endoplasmic reticulum stress; Porcine parvovirus; Protein kinase R-like ER kinase pathway; Unfolded protein response