Journal
JOURNAL OF VIROLOGY
Volume 79, Issue 19, Pages 12205-12217Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.79.19.12205-12217.2005
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Funding
- NIAID NIH HHS [R01 AI020211, R01 AI20211, 5F32AI056959, F32 AI056959] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007365, T32GM07365] Funding Source: Medline
- NINDS NIH HHS [F30NS051109, F30 NS051109] Funding Source: Medline
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Human cytomegalovirus carries a mitochondria-localized inhibitor of apoptosis (vMIA) that is conserved in primate cytomegaloviruses. We find that inactivating mutations within UL37x1, which encodes vMIA, do not substantially affect replication in Townevar ATCC (Towne-BAC), a virus that carries a functional copy of the betaherpesvirus-conserved viral inhibitor of caspase 8 activation, the UL36 gene product. In Towne-BAC infection, vMIA reduces susceptibility of infected cells to intrinsic death induced by proteasome inhibition. vMIA is sufficient to confer resistance to proteasome inhibition when expressed independent of viral infection. Murine cytomegalovirus m38.5, whose position in the viral genome is analogous to UL37x1, exhibits mitochondria) association and functions in much the same manner as vMIA in inhibiting intrinsic cell death. This work suggests a common role for vMIA in rodent and primate cytomegaloviruses, modulating the threshold of virus-infected cells to intrinsic cell death.
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