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Short Communication |

School of Biomedical and Molecular Sciences, University of Surrey, Guildford GU2 7XH, UK
Correspondence
Michael J. Carter
m.carter{at}surrey.ac.uk
Previous studies have identified virus proteins that traffic to mitochondria and may affect mitochondrial function. Here, it is reported that Human herpesvirus 1 (HHV-1, herpes simplex virus 1) and influenza virus reduced mitochondrial respiration, whilst Measles virus, cytomegalovirus, coxsackievirus B4 and Feline calicivirus did not. The inhibition of total cellular respiration was caused by a block in the mitochondrial electron-transport chain. This effect occurred during
-phase protein synthesis and the inhibition of mitochondrial respiration could be reproduced by ectopic expression of the
-phase protein US3. An HHV-1 mutant lacking this protein failed to inhibit oxygen consumption in infected cells relative to controls. It was concluded that US3 was mediating the suppression of mitochondrial respiration following HHV-1 infection. The integrity of the electron-transport chain in HHV-1-infected cells was analysed further and the site of the block in electron transport was located between complexes II and III, a site previously shown to be affected by Poliovirus.
Present address: Cancer Research UK, London EC1M 6BQ, UK.
This article has been cited by other articles:
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