tetano
Editor, Senior Moderator
Viruses
. 2021 Nov 1;13(11):2199.
doi: 10.3390/v13112199.
Apoptosis Enhances the Replication of Human Coronavirus OC43
Sony Maharjan[SUP] 1 [/SUP], Mijeong Kang[SUP] 2 [/SUP], Jinsoo Kim[SUP] 2 [/SUP], Dongbum Kim[SUP] 1 [/SUP], Sangkyu Park[SUP] 3 [/SUP], Minyoung Kim[SUP] 2 [/SUP], Kyeongbin Baek[SUP] 2 [/SUP], Younghee Lee[SUP] 3 [/SUP], Hyung-Joo Kwon[SUP] 1 2 [/SUP]
Affiliations
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.
Keywords: HCoV-OC43; apoptosis; replication.
. 2021 Nov 1;13(11):2199.
doi: 10.3390/v13112199.
Apoptosis Enhances the Replication of Human Coronavirus OC43
Sony Maharjan[SUP] 1 [/SUP], Mijeong Kang[SUP] 2 [/SUP], Jinsoo Kim[SUP] 2 [/SUP], Dongbum Kim[SUP] 1 [/SUP], Sangkyu Park[SUP] 3 [/SUP], Minyoung Kim[SUP] 2 [/SUP], Kyeongbin Baek[SUP] 2 [/SUP], Younghee Lee[SUP] 3 [/SUP], Hyung-Joo Kwon[SUP] 1 2 [/SUP]
Affiliations
- PMID: 34835005
- 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.
Keywords: HCoV-OC43; apoptosis; replication.