Institute of Medical Science, College of Medicine, Hallym University, Chuncheon 24252, Korea.
Department of Microbiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.
Viruses. 2021 Nov 1;13(11):2199. doi: 10.3390/v13112199.
Human coronavirus OC43 (HCoV-OC43) is one of the coronaviruses causing a mild common cold, but few studies have been made on this strain. Here, we identified the molecular mechanisms involved in HCoV-OC43-induced apoptosis and its implications for viral reproduction in Vero cells and MRC-5 cells. HCoV-OC43 infection induced apoptosis that was accompanied by cleavage of caspase-3 and PARP, degradation of cyclin D1, and cell cycle arrest at S and G2M phases. Dephosphorylation of STAT1 and STAT3, induced by HCoV-OC43 infection, was also associated with HCoV-OC43-mediated apoptosis. The pan-caspase inhibitor effectively prevented HCoV-OC43-induced apoptosis and reduced viral replication, suggesting that apoptosis contributes to viral replication. Collectively our results indicate that HCoV-OC43 induces caspase-dependent apoptosis to promote viral replication in Vero cells and MRC-5 cells.
人冠状病毒 OC43(HCoV-OC43)是引起轻度普通感冒的冠状病毒之一,但对该毒株的研究甚少。在这里,我们鉴定了 HCoV-OC43 诱导细胞凋亡的分子机制及其对 Vero 细胞和 MRC-5 细胞中病毒复制的影响。HCoV-OC43 感染诱导了伴随 caspase-3 和 PARP 切割、细胞周期蛋白 D1 降解以及 S 和 G2M 期细胞周期停滞的凋亡。HCoV-OC43 感染诱导的 STAT1 和 STAT3 去磷酸化也与 HCoV-OC43 介导的凋亡有关。泛半胱天冬酶抑制剂能有效阻止 HCoV-OC43 诱导的细胞凋亡并降低病毒复制,提示凋亡有助于病毒复制。总之,我们的结果表明 HCoV-OC43 通过诱导半胱天冬酶依赖性凋亡促进 Vero 细胞和 MRC-5 细胞中的病毒复制。