Apoptosis induced by the SARS-associated coronavirus in Vero cells is replication-dependent and involves caspase.

The pathogenesis of the severe acute respiratory syndrome (SARS), a newly emerging life-threatening disease in humans, remains unknown. It is believed that the modulation of apoptosis is relevant to diseases that are caused by various viruses. To examine potential apoptotic mechanisms related to SARS, we investigated features of apoptosis induced by the SARS-associated coronavirus (SARS-CoV) in host cells. The results indicated that the SARS-CoV-induced apoptosis in Vero cells in a virus replication-dependent manner. Additionally, the downregulation of Bcl-2, the activation of casapse 3, as well as the upregulation of Bax were detected, suggesting the involvement of the caspase family and the activation of the mitochondrial signaling pathway. Although there is a positive correlation between apoptosis and virus replication, the latter is not significantly blocked by treatment with the caspase inhibitor z-DEVD-FMK. These preliminary data provide important information on both the pathogenesis and potential antiviral targets of SARS-CoV.