Apoptosis Enhances the Replication of Human Coronavirus OC43

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. HC...

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Bibliographic Details
Published in:Viruses 2021-11, Vol.13 (11), p.2199
Main Authors: Maharjan, Sony, Kang, Mijeong, Kim, Jinsoo, Kim, Dongbum, Park, Sangkyu, Kim, Minyoung, Baek, Kyeongbin, Lee, Younghee, Kwon, Hyung-Joo
Format: Article
Language:English
Subjects:
Apoptosis
Caspase inhibitors
Caspase-3
Cell culture
Cell cycle
Common cold
Coronaviruses
Cyclin D1
Dephosphorylation
HCoV-OC43
Infections
Middle East respiratory syndrome
Molecular modelling
Mortality
Poly(ADP-ribose) polymerase
Replication
Respiratory diseases
Severe acute respiratory syndrome coronavirus 2
Stat1 protein
Stat3 protein
Vero cells
Viruses
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Summary: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.
ISSN:1999-4915
1999-4915
DOI:10.3390/v13112199