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细胞凋亡增强人类冠状病毒 OC43 的复制。

Apoptosis Enhances the Replication of Human Coronavirus OC43.

机构信息

Institute of Medical Science, College of Medicine, Hallym University, Chuncheon 24252, Korea.

Department of Microbiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.

出版信息

Viruses. 2021 Nov 1;13(11):2199. doi: 10.3390/v13112199.

Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f89d/8619903/03306f14d5cc/viruses-13-02199-g001.jpg

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