Jiyu Zhang, Liaoyuan Zhang, Hongyan Shi, Shufeng Feng , Tingshuai Feng, Jianfei Chen, Xin Zhang, Yuru Han, Jianbo Liu, Yiming Wang, Zhaoyang Ji, Zhaoyang Jing, Dakai Liu, Da Shi, Li Feng

Virology.2021 Oct 30;565:96-105.doi: 10.1016/j.virol.2021.10.009. Online ahead of print.

Abstract

Swine acute diarrhea syndrome coronavirus (SADS-CoV) is a newly discovered enteric coronavirus. We have previously shown that the caspase-dependent FASL-mediated and mitochondrion-mediated apoptotic pathways play a central role in SADS-CoV-induced apoptosis, which facilitates viral replication. However, the roles of intracellular signaling pathways in SADS-CoV-mediated cell apoptosis and the relative advantages that such pathways confer on the host or virus remain largely unknown. In this study, we show that SADS-CoV induces the activation of ERK during infection, irrespective of viral biosynthesis. The knockdown or chemical inhibition of ERK1/2 significantly suppressed viral protein expression and viral progeny production. The inhibition of ERK activation also circumvented SADS-CoV-induced apoptosis. Taken together, these data suggest that ERK activation is important for SADS-CoV replication, and contributes to the virus-mediated changes in host cells. Our findings demonstrate the takeover of a particular host signaling mechanism by SADS-CoV and identify a potential approach to inhibiting viral spread.

Keywords: Apoptosis; ERK pathway; Swine acute diarrhea syndrome coronavirus (SADS-CoV); Viral replication.

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