PKR protein kinase is activated by hepatitis C virus and inhibits viral replication through translational control
- Authors
- Kang, Ju-Il; Kwon, Shi-Nae; Park, Se-Hoon; Kim, Yun Ki; Choi, Sang-Yun; Kim, Jungsuh P.; Ahn, Byung-Yoon
- Issue Date
- Jun-2009
- Publisher
- ELSEVIER
- Keywords
- Hepatitis C virus; JFH1; PKR; eIF2 alpha phosphorylation; Translational control; Interferon
- Citation
- VIRUS RESEARCH, v.142, no.1-2, pp.51 - 56
- Indexed
- SCIE
SCOPUS
- Journal Title
- VIRUS RESEARCH
- Volume
- 142
- Number
- 1-2
- Start Page
- 51
- End Page
- 56
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/119929
- DOI
- 10.1016/j.virusres.2009.01.007
- ISSN
- 0168-1702
- Abstract
- Hepatitis C virus (HCV) infection is currently treated with IFN alpha-based therapy but little is known how IFN alpha inhibits HCV replication. We show here that HCV JFH1 infection of human hepatoma Huh-7 cells leads to the activation of IFN-inducible protein kinase PKR and phosphorylation of the translation initiation factor eIF2 alpha. Compared to a control cell HCV replication was significantly elevated in a PKR-knockdown cell, giving rise to a 10-fold higher viral titer, and was less sensitive to IFN alpha treatment. Conversely, transient expression of PKR inhibited HCV replication in a kinase-dependent manner with concomitant increase of eIF2 alpha phosphorylation. Further, expression of a phospho-mimetic eIF2 alpha mutant moderately inhibited HCV replication. Together, these results demonstrate that PKR is activated by HCV infection and plays a critical antiviral role through inhibition of viral protein translation. (C) 2009 Elsevier B.V. All rights reserved.
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Collections - Graduate School > Department of Life Sciences > 1. Journal Articles
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