期刊
VIROLOGY
卷 559, 期 -, 页码 196-209出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2021.04.007
关键词
PDCoV; SAPKs; Signal transduction; Cytokines; Viral replication
类别
资金
- Basic Science Research Programs through the National Research Foundation of Korea (NRF) - Ministry of Education [NRF-2015R1D1A1A09057406]
The JNK1/2 and p38 MAPK signaling pathways play important roles in viral biosynthesis and immune responses, thereby favoring the replication of PDCoV.
This study was conducted to examine the role of stress-activated protein kinases (SAPKs), including c-Jun NH2terminal 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.
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