title: Human cytomegalovirus infection increases mitochondrial biogenesis.
abstract: 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.
authors: Department of Microbiology, Oslo, Norway.
authors: Mari
authors: M
authors: Kaarbø
authors: Eirill
authors: E
authors: Ager-Wick
authors: Pia Øistad
authors: PØ
authors: Osenbroch
authors: Anette
authors: A
authors: Kilander
authors: Ragnhild
authors: R
authors: Skinnes
authors: Fredrik
authors: F
authors: Müller
authors: Lars
authors: L
authors: Eide
mesh_terms: D019069:Cell Respiration; D003586:Cytomegalovirus Infections / Q000503:physiopathology*; D005347:Fibroblasts / Q000648:ultrastructure / Q000821:virology*; D006801:Humans; D017874:Immediate-Early Proteins / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism* / Q000648:ultrastructure
chemical_list: D017874:Immediate-Early Proteins; C420323:UL37 protein, Human herpesvirus 5