Apoptosis Enhances the Replication of Human Coronavirus OC43

被引:10
作者
Maharjan, Sony [1 ]
Kang, Mijeong [2 ]
Kim, Jinsoo [2 ]
Kim, Dongbum [1 ]
Park, Sangkyu [3 ]
Kim, Minyoung [2 ]
Baek, Kyeongbin [2 ]
Lee, Younghee [3 ]
Kwon, Hyung-Joo [1 ,2 ]
机构
[1] Hallym Univ, Coll Med, Inst Med Sci, Chunchon 24252, South Korea
[2] Hallym Univ, Coll Med, Dept Microbiol, Chunchon 24252, South Korea
[3] Chungbuk Natl Univ, Coll Nat Sci, Dept Biochem, Cheongju 28644, South Korea
来源
VIRUSES-BASEL | 2021年 / 13卷 / 11期
基金
新加坡国家研究基金会;
关键词
HCoV-OC43; apoptosis; replication; CELL-DEATH; CALU-3; CELLS; VIRUS; INFECTION; CASPASES; ACTIVATION; STAT3; SARS; INDUCTION; AUTOPHAGY;
D O I
10.3390/v13112199
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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.
引用
收藏
页数:15
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