Bcl-2 and Bcl-xL overexpression inhibits cytochrome c release, activation of multiple caspases, and virus release following coxsackievirus B3 infection.
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| Abstract |
Coxsackievirus B3, a cytopathic virus in the family Picornaviridae, induces degenerative changes in host cell morphology. Here we demonstrate cytochrome c release and caspases-2, -3, -6, -7, -8, and -9 processing. Enforced Bcl-2 and Bcl-xL expression markedly reduced release of cytochrome c, presentation of the mitochondrial epitope 7A6, and depressed caspase activation following infection. In comparison, cell death using TRAIL ligand caused caspase-8 processing prior to cytochrome c release and executioner caspases and cell death was only partially rescued by Bcl-2 and Bcl-xL overexpression. Disruption of the mitochondrial inner membrane potential following CVB3 infection was not inhibited by zVAD.fmk treatment. Bcl-2 or Bcl-xL overexpression or zVAD.fmk treatment delayed the loss of host cell viability and decreased progeny virus release following infection. Our data suggest that mitochondrial release of cytochrome c may be an important early event in caspase activation in CVB3 infection, and, as such, may contribute to the loss of host-cell viability and progeny virus release.
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| Authors | Christopher M Carthy, Bobby Yanagawa, Honglin Luo, David J Granville, Decheng Yang, Paul Cheung, Caroline Cheung, Mitra Esfandiarei, Charles M Rudin, Craig B Thompson, David W C Hunt, Bruce M McManus |
| Journal | Virology (Virology) Vol. 313 Issue 1 Pg. 147-57 (Aug 15 2003) ISSN: 0042-6822 [Print] United States |
| PMID | 12951029 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't) |
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