Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics

Arch Virol. 2006 Feb;151(2):369-77. doi: 10.1007/s00705-005-0632-8. Epub 2005 Sep 12.

Abstract

Vero cells transfected with either neo- or bcl-2-plasmid were infected with SARS-CoV at a high multiplicity of infection. Apoptosis appeared after the onset of CPE and completion of virus replication, and could be prevented by Bcl-2 expression. Apoptosis is likely mediated by the mitochondrial pathway, as demonstrated by its inhibition using Bcl-2, and by the activation of the caspase cascade, resulting in PARP cleavage. Prevention of apoptosis did not affect susceptibility to infection, kinetics and extent of viral replication and release, thus implying that apoptosis is not involved in facilitating release and/or dissemination of SARS-CoV in Vero cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Caspases / metabolism*
  • Chlorocebus aethiops
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Severe acute respiratory syndrome-related coronavirus / pathogenicity*
  • Severe acute respiratory syndrome-related coronavirus / physiology*
  • Time Factors
  • Vero Cells
  • Virus Replication*

Substances

  • Proto-Oncogene Proteins c-bcl-2
  • Caspases