Apoptosis Enhances the Replication of Human Coronavirus OC43

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.

Keywords: HCoV-OC43; apoptosis; replication.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Caspase Inhibitors / pharmacology
  • Caspases / metabolism
  • Cell Line
  • Cell Proliferation
  • Chlorocebus aethiops
  • Coronavirus OC43, Human / drug effects
  • Coronavirus OC43, Human / physiology*
  • Humans
  • Interferon alpha-2 / pharmacology
  • Phosphorylation
  • STAT1 Transcription Factor / metabolism
  • STAT3 Transcription Factor / metabolism
  • Vero Cells
  • Viral Load
  • Virus Replication*

Substances

  • Caspase Inhibitors
  • Interferon alpha-2
  • STAT1 Transcription Factor
  • STAT3 Transcription Factor
  • Caspases