| Literature DB >> 20797756 |
Goki Suda1, Naoya Sakamoto, Yasuhiro Itsui, Mina Nakagawa, Megumi Tasaka-Fujita, Yusuke Funaoka, Takako Watanabe, Sayuri Nitta, Kei Kiyohashi, Seishin Azuma, Sei Kakinuma, Kiichiro Tsuchiya, Michio Imamura, Nobuhiko Hiraga, Kazuaki Chayama, Mamoru Watanabe.
Abstract
Mechanisms of difference in interferon sensitivity between hepatitis C virus (HCV) strains have yet to be clarified. Here, we constructed an infectious genotype2b clone and analyzed differences in interferon-alpha sensitivity between HCV-2b and 2a-JFH1 clones using intergenotypic homologous recombination. The HCV-2b/JFH1 chimeric virus able to infect Huh7.5.1 cells and was significantly more sensitive to IFN than JFH1. IFN-induced expression of MxA and 25-OAS was significantly lower in JFH1 than in 2b/JFH1-infected cells. In JFH1-infected cells, expression of SOCS3 and its inducer, IL-6, was significantly higher than in 2b/JFH1-infected cells. The IFN-resistance of JFH1 cells was negated by siRNA-knock down of SOCS3 expression and by pretreatment with anti-IL6 antibody. In conclusion, intergenotypic differences of IFN sensitivity of HCV may be attributable to the sequences of HCV structural proteins and can be determined by SOCS3 and IL-6 expression levels.Entities:
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Year: 2010 PMID： 20797756 DOI： 10.1016/j.virol.2010.07.041
Source DB: PubMed Journal: Virology ISSN： 0042-6822 Impact factor: 3.616