1. Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics
- Author
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Licia Bordi, Concetta Castilletti, Mauro Piacentini, Giuseppe Ippolito, Alessandra Rinaldi, Maria Rosaria Capobianchi, Fabiola Ciccosanti, Gabriella Rozera, S. Calcaterra, Laura Falasca, S. Zaniratti, and A. Di Caro
- Subjects
Programmed cell death ,Time Factors ,viruses ,Infectious Disease ,Apoptosis ,Virus Replication ,Caspase-Dependent Apoptosis ,Virus ,Multiplicity of infection ,PARP Cleavage ,Virology ,Chlorocebus aethiops ,Animals ,Vero Cells ,Caspase ,biology ,Brief Report ,General Medicine ,Mitochondrial Pathway ,Viral replication ,Proto-Oncogene Proteins c-bcl-2 ,Severe acute respiratory syndrome-related coronavirus ,Caspases ,biology.protein ,Vero cell ,Vero Cell - Abstract
Summary. 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.
- Published
- 2005