Chen Li, Ni Minshu, Ahmed Waqas, Xu Yue, Bao Xi, Zhuang Tenghan, Feng Lei, Guo Meijin
State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai, PR China.
Institute of Veterinary Immunology & Engineering, National Research Center of Engineering and Technology for Veterinary Biologicals, Jiangsu Academy of Agricultural Sciences, Nanjing, Jiangsu, PR China.
J Gen Virol. 2022 Dec;103(12). doi: 10.1099/jgv.0.001818.
Viral infections cause endoplasmic reticulum (ER) stress and subsequently unfolded protein response (UPR) which restores ER homeostasis. In this study, levels of proteins or transcription of three UPR pathways were examined in suspension-cultured BHK-21 cells to investigate Pseudorabies virus (PRV) infection-induced ER stress, in which glucose-related proteins 78 kD and 94 kD (GRP78 and GRP94) were upregulated. The downstream double-stranded RNA-activated protein kinase-like ER kinase (PERK) pathway was activated with upregulation of ATF4, CHOP, and GADD34, and the inositol requiring kinase 1 (IRE1) pathway was triggered by the splicing of X box-binding protein 1 (XBP1) mRNA and the enhanced expression of p58 and EDEM. Furthermore, our results showed that the ER stress, induced by 0.005 µM thapsigargin, promoted PRV replication in suspension-cultured BHK-21 cells, and that PRV glycoprotein B (gB) overexpression triggered the PERK and IRE1 pathways.
病毒感染会引发内质网（ER）应激，随后引发未折叠蛋白反应（UPR），从而恢复内质网的稳态。在本研究中，检测了悬浮培养的BHK - 21细胞中三条UPR途径的蛋白质水平或转录情况，以研究伪狂犬病病毒（PRV）感染诱导的内质网应激，其中葡萄糖相关蛋白78 kD和94 kD（GRP78和GRP94）上调。下游双链RNA激活的蛋白激酶样内质网激酶（PERK）途径通过ATF4、CHOP和GADD34的上调而被激活，肌醇需求激酶1（IRE1）途径则由X盒结合蛋白1（XBP1）mRNA的剪接以及p58和EDEM表达增强所触发。此外，我们的结果表明，0.005 μM毒胡萝卜素诱导的内质网应激促进了悬浮培养的BHK - 21细胞中PRV的复制，并且PRV糖蛋白B（gB）的过表达触发了PERK和IRE1途径。
