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Virology. 2010 Oct 25;406(2):336-41. doi: 10.1016/j.virol.2010.07.039. Epub 2010 Aug 13.

An important role of the heat shock response in infected cells for replication of baculoviruses.

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  • 1N.K. Koltzov Institute of Developmental Biology, Russian Academy of Sciences, 26 Vavilova Str., Moscow 119991, Russia.

Abstract

Baculoviruses serve as a stress factor that can activate both death-inducing and cytoprotective pathways in infected cells. In this report, induction of heat shock proteins (HSPs) of the 70-kDa family (HSP/HSC70) in Sf-9 cells after infection with AcMNPV was monitored by Western blot analysis. Two-dimensional electrophoresis in polyacrylamide gel revealed changes in the cellular pattern of HSP/HSC70s and synthesis of a new member of the HSP/HSC70 family in the infected cells. Although infection with AcMNPV moderately increased the HSP/HSC70 content in cells under standard conditions, the infection potentiated the response to heat shock boosting the HSP/HSC70s content in infected cells several-fold in comparison with uninfected cells. Addition of KNK437, a known inhibitor of inducible HSPs, decreased the rate of viral DNA synthesis in infected cells more than one order of magnitude and markedly suppressed the release of budded viruses indicating the importance of the heat shock response for baculovirus replication.

Copyright © 2010 Elsevier Inc. All rights reserved.

PMID:
20708767
[PubMed - indexed for MEDLINE]
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