Journal
JOURNAL OF VIROLOGY
Volume 77, Issue 1, Pages 631-641Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.77.1.631-641.2003
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI020211, F32AI009855] Funding Source: NIH RePORTER
- NIAID NIH HHS [R01 AI020211, R01 AI20211, F32 AI09855, F32 AI009855] Funding Source: Medline
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By 24 h after infection with human cytomegalovirus, the reticular mitochondrial network characteristic of uninfected fibroblasts was disrupted as mitochondria became punctate and dispersed. These alterations were associated with expression of the immediate-early (a) antiapoptotic UL37x1 gene product viral mitochondrion-localized inhibitor of apoptosis (vMIA). Similar alterations in mitochondrial morphology were induced directly by vMIA in transfected cells. A 68-amino-acid antiapoptotic derivative of vMIA containing the mitochondrial localization and antiapoptotic domains also induced disruption, whereas a mutant lacking the antiapoptotic domain failed to cause disruption. These data suggest that the fission and/or fusion process that normally controls mitochondrial networks is altered by vMIA. Mitochondrial fission has been implicated in the induction of apoptosis and vMIA-mediated inhibition of apoptosis may occur subsequent to this event.
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