Stress-activated protein kinases are involved in the replication of porcine deltacoronavirus

Abstract

This study was conducted to examine the role of stress-activated protein kinases (SAPKs), including c-Jun NH2-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.