Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.virol.2014.10.027
Title: NS5B induces up-regulation of the BH3-only protein, BIK, essential for the Hepatitis C virus RNA replication and viral release
Authors: Aweya, Jude Juventus
Sze, Ching Wooen 
Bayega, Anthony
Mohd-Ismail, Nur Khairiah
Lin, Deng
Hotta, Hak
Tan, Yee-Joo 
Keywords: Hepatitis C virus (HCV); BIK; NS5B
Issue Date: 1-Jan-2015
Publisher: Elsevier
Citation: Aweya, Jude Juventus, Sze, Ching Wooen, Bayega, Anthony, Mohd-Ismail, Nur Khairiah, Lin, Deng, Hotta, Hak, Tan, Yee-Joo (2015-01-01). NS5B induces up-regulation of the BH3-only protein, BIK, essential for the Hepatitis C virus RNA replication and viral release. Virology 474 : 41-51. ScholarBank@NUS Repository. https://doi.org/10.1016/j.virol.2014.10.027
Abstract: Hepatitis C virus (HCV) induces cytopathic effects in the form of hepatocytes apoptosis thought to be resulted from the interaction between viral proteins and host factors. Using pathway specific PCR array, we identified 9 apoptosis-related genes that are dysregulated during HCV infection, of which the BH3-only pro-apoptotic Bcl-2 family protein, BIK, was consistently up-regulated at the mRNA and protein levels. Depletion of BIK protected host cells from HCV-induced caspase-3/7 activation but not the inhibitory effect of HCV on cell viability. Furthermore, viral RNA replication and release were significantly suppressed in BIK-depleted cells and over-expression of the RNA-dependent RNA polymerase, NS5B, was able to induce BIK expression. Immunofluorescence and co-immunoprecipitation assays showed co-localization and interaction of BIK and NS5B, suggesting that BIK may be interacting with the HCV replication complex through NS5B. These results imply that BIK is essential for HCV replication and that NS5B is able to induce BIK expression.
Source Title: Virology
URI: http://scholarbank.nus.edu.sg/handle/10635/122542
ISSN: 00426822
DOI: 10.1016/j.virol.2014.10.027
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