Restriction of human herpesvirus 6B replication by p53

The Journal of General Virology
Bodil ØsterPer Höllsberg

Abstract

Human herpesvirus 6B (HHV-6B) induces significant accumulation of p53 in both the nucleus and cytoplasm during infection. Activation of p53 by DNA damage is known to induce either growth arrest or apoptosis; nevertheless, HHV-6B-infected cells are arrested in their cell cycle independently of p53, and only a minor fraction of the infected cells undergoes apoptosis. Using pifithrin-alpha, a p53 inhibitor, and p53-null cells, this study showed that infected epithelial cells accumulated viral transcripts and proteins to a significantly higher degree in the absence of active p53. Moreover, HHV-6B-induced cytopathic effects were greatly enhanced in the absence of p53. This suggests that, in epithelial cells, some of the functions of p53 leading to cell-cycle arrest and apoptosis are restrained by HHV-6B infection, whereas other cellular defences, causing inhibition of virus transcription, are partially retained.

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Citations

Sep 10, 2008·Molecular and Cellular Biology·Manabu TauraHirofumi Kai
Jan 17, 2009·Cell Division·Adam J Hume, Robert F Kalejta
Jul 30, 2011·Future Virology·Christopher M TraylenShaw M Akula
Jul 5, 2011·Reviews in Medical Virology·Pedro A Lazo, Claudio R Santos
Jul 22, 2010·Journal of Medical Virology·Louis FlamandDharam V Ablashi
Sep 23, 2010·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Aurélie LacroixSylvie Ranger-Rogez

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