Jeon Ji Hyun, Lee Changhee
Animal Virology Laboratory, School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 702-701, Republic of Korea.
Animal Virology Laboratory, School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 702-701, Republic of Korea.
Virology. 2021 Jul;559:196-209. doi: 10.1016/j.virol.2021.04.007. Epub 2021 May 3.
This study was conducted to examine the role of stress-activated protein kinases (SAPKs), including c-Jun NH-terminal kinases (JNK1/2) and p38 mitogen-activated protein kinase (MAPK), in porcine deltacoronavirus (PDCoV) infection. Results demonstrated the activation of JNK1/2 and p38 MAPK in PDCoV-infected cells, which occurred concomitant with viral biosynthesis and irrespective of cell type. Pharmacological inhibition or knockdown of either SAPK significantly attenuated PDCoV replication, whereas addition of a signaling activator augmented virus infectivity. Moreover, pharmacological inhibition of JNK1/2 or p38 MAPK activation was innocuous to viral entry but significantly detrimental to post uncoating stages of the replication cycle. Remarkably, cytokine gene expression in PDCoV-infected IPEC-J2 cells was modified by inhibiting the activation of either SAPK. Collectively, these data indicate that JNK1/2 and p38 MAPK signaling pathways contribute to viral biosynthesis and regulate immune responses, thereby favoring the replication of PDCoV.
本研究旨在探讨应激激活蛋白激酶（SAPKs），包括c-Jun氨基末端激酶（JNK1/2）和p38丝裂原活化蛋白激酶（MAPK）在猪德尔塔冠状病毒（PDCoV）感染中的作用。结果表明，在PDCoV感染的细胞中JNK1/2和p38 MAPK被激活，这与病毒生物合成同时发生且与细胞类型无关。对任一SAPK进行药理学抑制或敲低均可显著减弱PDCoV复制，而添加信号激活剂则增强病毒感染性。此外，对JNK1/2或p38 MAPK激活的药理学抑制对病毒进入无害，但对复制周期的脱壳后阶段有显著损害。值得注意的是，通过抑制任一SAPK的激活可改变PDCoV感染的IPEC-J2细胞中细胞因子基因的表达。总体而言，这些数据表明JNK1/2和p38 MAPK信号通路有助于病毒生物合成并调节免疫反应，从而有利于PDCoV的复制。
