Human cytomegalovirus infection increases mitochondrial biogenesis

Mitochondrion. 2011 Nov;11(6):935-45. doi: 10.1016/j.mito.2011.08.008. Epub 2011 Sep 2.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Respiration
  • Cytomegalovirus Infections / physiopathology*
  • Fibroblasts / ultrastructure
  • Fibroblasts / virology*
  • Humans
  • Immediate-Early Proteins / metabolism
  • Mitochondria / metabolism*
  • Mitochondria / ultrastructure

Substances

  • Immediate-Early Proteins
  • UL37 protein, Human herpesvirus 5