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Mol. Cells 2011; 32(2): 167-172
Published online June 23, 2011
https://doi.org/10.1007/s10059-011-1059-6
© The Korean Society for Molecular and Cellular Biology
PKR-Dependent Mechanisms of Interferon-α for Inhibiting Hepatitis B Virus Replication
Il-Hyun Park1,2, Kyung-Won Baek1,2, Eun-Young Cho1, and Byung-Yoon Ahn1,*
Correspondence to : *Correspondence: ahnbyung@korea.ac.kr
Interferon-alpha (IFN-alpha) inhibits the replication of hepatitis B virus (HBV) in vivo and in vitro, but the molecular mechanism of this inhibition has been elusive. We found that while HBV replication in transfected human hepatoma Huh-7 cell was severely inhibited by IFN-alpha treatment as reported previously, this inhibition was markedly impaired in the cell in which the expression of IFN-inducible, double-stranded RNA-dependent protein kinase (PKR) was stably and spe-cifically suppressed through RNA-interfer-ence. Intracellular level of viral capsids was down-regu-lated likewise in a PKR-dependent manner, whereas that of HBV transcripts including the viral RNA pregenome was not affected by IFN-alpha treatment. Ectopic expression of PKR also resulted in the reduction of viral capsids with concomitant increase of phosphorylated eIF2alpha. These results suggested that PKR functions as a key mediator of IFN-alpha in opposing HBV replication, most likely through the inhibition of protein synthesis.
Keywords antiviral mechanism, Hepatitis B virus, IFN-α, PKR
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Research Article
Mol. Cells 2011; 32(2): 167-172
Published online August 31, 2011 https://doi.org/10.1007/s10059-011-1059-6
Copyright © The Korean Society for Molecular and Cellular Biology.
PKR-Dependent Mechanisms of Interferon-α for Inhibiting Hepatitis B Virus Replication
Il-Hyun Park1,2, Kyung-Won Baek1,2, Eun-Young Cho1, and Byung-Yoon Ahn1,*
1School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Korea, 2These authors contributed equally to this work.
Correspondence to:*Correspondence: ahnbyung@korea.ac.kr
Abstract
Interferon-alpha (IFN-alpha) inhibits the replication of hepatitis B virus (HBV) in vivo and in vitro, but the molecular mechanism of this inhibition has been elusive. We found that while HBV replication in transfected human hepatoma Huh-7 cell was severely inhibited by IFN-alpha treatment as reported previously, this inhibition was markedly impaired in the cell in which the expression of IFN-inducible, double-stranded RNA-dependent protein kinase (PKR) was stably and spe-cifically suppressed through RNA-interfer-ence. Intracellular level of viral capsids was down-regu-lated likewise in a PKR-dependent manner, whereas that of HBV transcripts including the viral RNA pregenome was not affected by IFN-alpha treatment. Ectopic expression of PKR also resulted in the reduction of viral capsids with concomitant increase of phosphorylated eIF2alpha. These results suggested that PKR functions as a key mediator of IFN-alpha in opposing HBV replication, most likely through the inhibition of protein synthesis.
Keywords: antiviral mechanism, Hepatitis B virus, IFN-α, PKR
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