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Herpes Research Today is a free monthly online journal that collates and summarizes the latest research about Herpes, including details on herpes simplex virus (hsv), genital, oral, symptoms, treatment.


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Protection against heat and staurosporine mediated apoptosis by the HSV-1 US11 protein.

Javouhey E, Gibert B, Arrigo AP, Diaz JJ, Diaz-Latoud C

Laboratoire Stress, chaperons et mort cellulaire, Université de Lyon, Lyon, F-69003, France.

US11 protein, one of herpes simplex virus type 1 (HSV-1) true late gene products, plays a role in the virally induced post-transcriptional control of gene expression. In addition, US11 expression also interferes with the cellular response to HSV-1 infection that can lead to apoptosis. We have previously shown that US11 expression enhanced the recovery of cellular protein synthesis and increased cell survival in response to thermal stress. Since heat shock can activate apoptosis, we tested for a possible anti-apoptotic behavior of US11. Here, we show that, in HeLa cells, US11 expression strongly reduced heat induced apoptosis, a phenomenon independent of Hsp expression and characterized by a delayed cytochrome c efflux from mitochondria and reduced caspase 3 activation. Moreover, US11 expression also protected against staurosporine induced apoptosis. Hence, our results favor an anti-apoptotic activity of US11 polypeptide that appears to be located at the level of mitochondria or upstream signaling pathways.

Published 26 May 2008 in Virology, 376(1): 31-41.
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