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PKR-dependent mechanisms of interferon-alpha for inhibiting hepatitis B virus replication

Authors
Park, Il-HyunBaek, Kyung-WonCho, Eun-YoungAhn, Byung-Yoon
Issue Date
8월-2011
Publisher
KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
Keywords
antiviral mechanism; Hepatitis B virus; IFN-alpha; PKR
Citation
MOLECULES AND CELLS, v.32, no.2, pp.167 - 172
Indexed
SCIE
SCOPUS
KCI
Journal Title
MOLECULES AND CELLS
Volume
32
Number
2
Start Page
167
End Page
172
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/111866
DOI
10.1007/s10059-011-1059-6
ISSN
1016-8478
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 specifically suppressed through RNA-interference. Intracellular level of viral capsids was down-regulated 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 eIF2 alpha. 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.
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