Human cytomegalovirus infection increases mitochondrial biogenesis

Fibroblasts infected by Human Cytomegalovirus (CMV) undergo a robust increase in mitochondrial biogenesis with a corresponding increase in mitochondrial activity that is partly dependent on the viral anti-apoptotic pUL37x1 protein (vMIA). The increased respiration activity is blocked by the mitochon...

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Published inMitochondrion Vol. 11; no. 6; pp. 935 - 945
Main Authors Kaarbø, Mari, Ager-Wick, Eirill, Osenbroch, Pia Øistad, Kilander, Anette, Skinnes, Ragnhild, Müller, Fredrik, Eide, Lars
Format Journal Article
LanguageEnglish
Published Netherlands 01.11.2011
Subjects
Cell Respiration
Cytomegalovirus Infections - physiopathology
Fibroblasts - ultrastructure
Fibroblasts - virology
Human cytomegalovirus
Humans
Immediate-Early Proteins - metabolism
Mitochondria - metabolism
Mitochondria - ultrastructure
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Summary:Fibroblasts infected by Human Cytomegalovirus (CMV) undergo a robust increase in mitochondrial biogenesis with a corresponding increase in mitochondrial activity that is partly dependent on the viral anti-apoptotic pUL37x1 protein (vMIA). The increased respiration activity is blocked by the mitochondrial translation inhibitor chloramphenicol, which additionally suppresses viral production. Intriguingly, chloramphenicol and pUL37x1 depletion have different effects on respiration capacity but similar effects on CMV production, suggesting that pUL37x1 promotes viral replication by efficient utilization of new mitochondria. These results argue for a role of pUL37x1 beyond controlling apoptosis.
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ISSN:1567-7249
1872-8278
DOI:10.1016/j.mito.2011.08.008