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.
Original language | English (US) |
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Pages (from-to) | 147-157 |
Number of pages | 11 |
Journal | Virology |
Volume | 313 |
Issue number | 1 |
DOIs | |
State | Published - Aug 15 2003 |
Externally published | Yes |
Keywords
- Apoptosis
- Bcl-2
- Bcl-xL
- Caspase
- Coxsackievirus B3
- Cytochrome c
- Myocarditis
ASJC Scopus subject areas
- Virology
- Infectious Diseases