Mitochondrial Apoptosis and the Peripheral Benzodiazepine Receptor

Open Access
Publisher Website
Google Scholar
Abstract
The 18-kD M11L protein is a major virulence factor for myxomatosis. In vivo, M11L knockout viruses provoke a greatly reduced mortality and induce more vigorous, presumably host-protective inflammatory reactions than pathogenic wild-type strains. In vitro, M11L knockout viruses cause accelerated apoptosis in infected rabbit lymphocytes or monocytes, as compared with wild-type controls (2, 3), suggesting that M11L acts as an inhibitor of apoptosis. Overexpression of M11L suffices to inhibit apoptosis induced via a variety of nonviral inducers suggesting that it acts as general rather than a virus- or signal-specific apoptosis inhibitor (1).