start-ver=1.4
cd-journal=joma
no-vol=69
cd-vols=
no-issue=2
article-no=
start-page=71
end-page=78
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=201504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Annexin A1 Negatively Regulates Viral RNA Replication of Hepatitis C Virus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Persistent infection with hepatitis C virus (HCV) often causes chronic hepatitis, and then shows a high rate of progression to liver cirrhosis and hepatocellular carcinoma. To clarify the mechanism of the persistent HCV infection is considered to be important for the discovery of new target(s) for the development of anti-HCV strategies. In the present study, we found that the expression level of annexin A1 (ANXA1) in human hepatoma cell line Li23-derived D7 cells was remarkably lower than that in parental Li23 cells, whereas the susceptibility of D7 cells to HCV infection was much higher than that of Li23 cells. Therefore, we hypothesized that ANXA1 negatively regulates persistent HCV infection through the inhibition of viral RNA replication. The results revealed that HCV production was significantly inhibited without a concomitant reduction in the amount of lipid droplets in the D7 cells stably expressing exogenous ANXA1. Further, we demonstrated that ANXA1 negatively regulated the step of viral RNA replication rather than that of viral entry in human hepatocytes. These results suggest that ANXA1 would be a novel target for the development of anti-HCV strategies.
en-copyright=
kn-copyright=

en-aut-name=HiramotoHiroki
en-aut-sei=Hiramoto
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=DansakoHiromichi
en-aut-sei=Dansako
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakedaMidori
en-aut-sei=Takeda
en-aut-mei=Midori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SatohShinya
en-aut-sei=Satoh
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WakitaTakaji
en-aut-sei=Wakita
en-aut-mei=Takaji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KatoNobuyuki
en-aut-sei=Kato
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Virology II, National Institute of Infectious Disease

affil-num=6
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=HCV
kn-keyword=HCV
en-keyword=annexin A1
kn-keyword=annexin A1
en-keyword=Li23 cell line
kn-keyword=Li23 cell line
en-keyword=Li23-derived D7 cells
kn-keyword=Li23-derived D7 cells
en-keyword=HCV-JFH-1
kn-keyword=HCV-JFH-1
END

start-ver=1.4
cd-journal=joma
no-vol=122
cd-vols=
no-issue=1
article-no=
start-page=9
end-page=16
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The DNA damage sensors ataxia-telangiectasia mutated kinase and checkpoint kinase 2 are required for hepatitis C virus RNA replication
kn-title=DNA 損傷センサーATMキナーゼとChk2はＣ型肝炎ウイルスのRNA複製に必要である
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=AriumiYasuo
en-aut-sei=Ariumi
en-aut-mei=Yasuo
kn-aut-name=有海康雄
kn-aut-sei=有海
kn-aut-mei=康雄
aut-affil-num=1
ORCID=

en-aut-name=KurokiMisao
en-aut-sei=Kuroki
en-aut-mei=Misao
kn-aut-name=黒木美沙緒
kn-aut-sei=黒木
kn-aut-mei=美沙緒
aut-affil-num=2
ORCID=

en-aut-name=DansakoHiromichi
en-aut-sei=Dansako
en-aut-mei=Hiromichi
kn-aut-name=團迫浩方
kn-aut-sei=團迫
kn-aut-mei=浩方
aut-affil-num=3
ORCID=

en-aut-name=AbeKenichi
en-aut-sei=Abe
en-aut-mei=Kenichi
kn-aut-name=阿部健一
kn-aut-sei=阿部
kn-aut-mei=健一
aut-affil-num=4
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=池田正徳
kn-aut-sei=池田
kn-aut-mei=正徳
aut-affil-num=5
ORCID=

en-aut-name=WakitaTakaji
en-aut-sei=Wakita
en-aut-mei=Takaji
kn-aut-name=脇田隆字
kn-aut-sei=脇田
kn-aut-mei=隆字
aut-affil-num=6
ORCID=

en-aut-name=KatoNobuyuki
en-aut-sei=Kato
en-aut-mei=Nobuyuki
kn-aut-name=加藤宣之
kn-aut-sei=加藤
kn-aut-mei=宣之
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学

affil-num=6
en-affil=
kn-affil=国立感染症研究所　ウイルス第二部

affil-num=7
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学
en-keyword=HCV
kn-keyword=HCV
en-keyword=ATM
kn-keyword=ATM
en-keyword=Chk2
kn-keyword=Chk2
en-keyword=宿主因子
kn-keyword=宿主因子
en-keyword=DNA 損傷センサー
kn-keyword=DNA 損傷センサー
END

start-ver=1.4
cd-journal=joma
no-vol=430
cd-vols=
no-issue=2
article-no=
start-page=592
end-page=597
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130111
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=PML tumor suppressor protein is required for HCV production
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=PML tumor suppressor protein, which forms discrete nuclear structures termed PML-nuclear bodies, has been associated with several cellular functions, including cell proliferation, apoptosis and antiviral defense. Recently, it was reported that the HCV core protein colocalizes with PML in PML-NBs and abrogates the PML function through interaction with PML. However, role(s) of PML in HCV life cycle is unknown. To test whether or not PML affects HCV life cycle, we examined the level of secreted HCV core and the infectivity of HCV in the culture supernatants as well as the level of HCV RNA in HuH-7-derived RSc cells, in which HCV-JFH1 can infect and efficiently replicate, stably expressing short hairpin RNA targeted to PML. In this context, the level of secreted HCV core and the infectivity in the supernatants from PML knockdown cells was remarkably reduced, whereas the level of HCV RNA in the PML knockdown cells was not significantly affected in spite of very effective knockdown of PML. In fact, we showed that PML is unrelated to HCV RNA replication using the subgenomic HCV-JFH1 replicon RNA, JRN/3-5B. Furthermore, the infectivity of HCV-like particle in the culture supernatants was significantly reduced in PML knockdown JRN/3-5B cells expressing core to NS2 coding region of HCV-JFH1 genome using the trans-packaging system. Finally, we also demonstrated that INI1 and DDX5, the PML-related proteins, are involved in HCV production. Taken together, these findings suggest that PML is required for HCV production.
en-copyright=
kn-copyright=

en-aut-name=KurokiMisao
en-aut-sei=Kuroki
en-aut-mei=Misao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AriumiYasuo
en-aut-sei=Ariumi
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HijikataMakoto
en-aut-sei=Hijikata
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DansakoHiromichi
en-aut-sei=Dansako
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WakitaTakaji
en-aut-sei=Wakita
en-aut-mei=Takaji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ShimotohnoKunitada
en-aut-sei=Shimotohno
en-aut-mei=Kunitada
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KatoNobuyuki
en-aut-sei=Kato
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci

affil-num=3
en-affil=
kn-affil=Kyoto Univ, Dept Viral Oncol, Inst Virus Res

affil-num=4
en-affil=
kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci

affil-num=6
en-affil=
kn-affil=Natl Inst Infect Dis, Dept Virol 2

affil-num=7
en-affil=
kn-affil=Natl Ctr Global Hlth & Med, Res Ctr Hepatitis & Immunol

affil-num=8
en-affil=
kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci
en-keyword=Hepatitis C virus
kn-keyword=Hepatitis C virus
en-keyword=PML
kn-keyword=PML
en-keyword=INI1
kn-keyword=INI1
en-keyword=DDX5
kn-keyword=DDX5
en-keyword=Tumor suppressor
kn-keyword=Tumor suppressor
en-keyword=Lipid droplet
kn-keyword=Lipid droplet
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=3
article-no=
start-page=e91156
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140313
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Genetic Characterization of Hepatitis C Virus in Long-Term RNA Replication Using Li23 Cell Culture Systems
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background　
　
The most distinguishing genetic feature of hepatitis C virus (HCV) is its remarkable diversity and variation. To understand this feature, we previously performed genetic analysis of HCV in the long-term culture of human hepatoma HuH-7-derived HCV RNA-replicating cell lines. On the other hand, we newly established HCV RNA-replicating cell lines using human hepatoma Li23 cells, which were distinct from HuH-7 cells.
　
Methodology/Principal Findings　
　
Li23-derived HCV RNA-replicating cells were cultured for 4 years. We performed genetic analysis of HCVs recovered from these cells at 0, 2, and 4 years in culture. Most analysis was performed in two separate parts: one part covered from the 5′-terminus to NS2, which is mostly nonessential for RNA replication, and the other part covered from NS3 to NS5B, which is essential for RNA replication. Genetic mutations in both regions accumulated in a time-dependent manner, and the mutation rates in the 5′-terminus-NS2 and NS3-NS5B regions were 4.0–9.0×10−3 and 2.7–4.0×10−3 base substitutions/site/year, respectively. These results suggest that the variation in the NS3-NS5B regions is affected by the pressure of RNA replication. Several in-frame deletions (3–105 nucleotides) were detected in the structural regions of HCV RNAs obtained from 2-year or 4-year cultured cells. Phylogenetic tree analyses clearly showed that the genetic diversity of HCV was expanded in a time-dependent manner. The GC content of HCV RNA was significantly increased in a time-dependent manner, as previously observed in HuH-7-derived cell systems. This phenomenon was partially due to the alterations in codon usages for codon optimization in human cells. Furthermore, we demonstrated that these long-term cultured cells were useful as a source for the selection of HCV clones showing resistance to anti-HCV agents.
　
Conclusions/Significance　
　
Long-term cultured HCV RNA-replicating cells are useful for the analysis of evolutionary dynamics and variations of HCV and for drug-resistance analysis.
en-copyright=
kn-copyright=

en-aut-name=KatoNobuyuki
en-aut-sei=Kato
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SejimaHiroe
en-aut-sei=Sejima
en-aut-mei=Hiroe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UedaYouki
en-aut-sei=Ueda
en-aut-mei=Youki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoriKyoko
en-aut-sei=Mori
en-aut-mei=Kyoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SatohShinya
en-aut-sei=Satoh
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=DansakoHiromichi
en-aut-sei=Dansako
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=2015
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The cyclic GMP-AMP synthetase-STING signaling pathway is required for both the innate immune response against HBV and the suppression of HBV assembly
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=During viral replication, the innate immune response is induced through the recognition of viral replication intermediates by host factor(s). One of these host factors, cyclic GMP-AMP synthetase (cGAS), was recently reported to be involved in the recognition of viral DNA derived from DNA viruses. However, it is uncertain whether cGAS is involved in the recognition of hepatitis B virus (HBV), which is a hepatotropic DNA virus. In the present study, we demonstrated that HBV genome-derived dsDNA induced the innate immune response through cGAS and its adaptor protein, STING, in human hepatoma Li23 cells expressing high levels of cGAS. In addition, we demonstrated that HBV infection induced ISG56 through the cGAS-STING signaling pathway. This signaling pathway also showed an antiviral response towards HBV through the suppression of viral assembly. From these results, we conclude that the cGAS-STING signaling pathway is required for not only the innate immune response against HBV but also the suppression of HBV assembly. The cGAS-STING signaling pathway may thus be a novel target for anti-HBV strategies.
en-copyright=
kn-copyright=

en-aut-name=DansakoHiromichi
en-aut-sei=Dansako
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UedaYouki
en-aut-sei=Ueda
en-aut-mei=Youki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OkumuraNobuaki
en-aut-sei=Okumura
en-aut-mei=Nobuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SatohShinya
en-aut-sei=Satoh
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SugiyamaMasaya
en-aut-sei=Sugiyama
en-aut-mei=Masaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MizokamiMasashi
en-aut-sei=Mizokami
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KatoNobuyuki
en-aut-sei=Kato
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine

affil-num=6
en-affil=
kn-affil=Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine

affil-num=7
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry

affil-num=8
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
en-keyword=Antiviral response
kn-keyword=Antiviral response
en-keyword=hepatitis B virus
kn-keyword=hepatitis B virus
en-keyword=innate immune response
kn-keyword=innate immune response
en-keyword=cGAS-STING signaling pathway
kn-keyword=cGAS-STING signaling pathway
en-keyword=viral assembly
kn-keyword=viral assembly
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=8
article-no=
start-page=e72519
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130830
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=New Preclinical Antimalarial Drugs Potently Inhibit Hepatitis C Virus Genotype 1b RNA Replication
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=BACKGROUND: 

Persistent hepatitis C virus (HCV) infection causes chronic liver diseases and is a global health problem. Although new triple therapy (pegylated-interferon, ribavirin, and telaprevir/boceprevir) has recently been started and is expected to achieve a sustained virologic response of more than 70% in HCV genotype 1 patients, there are several problems to be resolved, including skin rash/ageusia and advanced anemia. Thus a new type of anti-HCV drug is still needed. 　

METHODOLOGY/PRINCIPAL FINDINGS: 　
　
Recently developed HCV drug assay systems using HCV-RNA-replicating cells (e.g., HuH-7-derived OR6 and Li23-derived ORL8) were used to evaluate the anti-HCV activity of drug candidates. During the course of the evaluation of anti-HCV candidates, we unexpectedly found that two preclinical antimalarial drugs (N-89 and its derivative N-251) showed potent anti-HCV activities at tens of nanomolar concentrations irrespective of the cell lines and HCV strains of genotype 1b. We confirmed that replication of authentic HCV-RNA was inhibited by these drugs. Interestingly, however, this anti-HCV activity did not work for JFH-1 strain of genotype 2a. We demonstrated that HCV-RNA-replicating cells were cured by treatment with only N-89. A comparative time course assay using N-89 and interferon-α demonstrated that N-89-treated ORL8 cells had more rapid anti-HCV kinetics than did interferon-α-treated cells. This anti-HCV activity was largely canceled by vitamin E. In combination with interferon-α and/or ribavirin, N-89 or N-251 exhibited a synergistic inhibitory effect.　
　
CONCLUSIONS/SIGNIFICANCE:　
　
We found that the preclinical antimalarial drugs N-89 and N-251 exhibited very fast and potent anti-HCV activities using cell-based HCV-RNA-replication assay systems. N-89 and N-251 may be useful as a new type of anti-HCV reagents when used singly or in combination with interferon and/or ribavirin.
en-copyright=
kn-copyright=

en-aut-name=UedaYouki
en-aut-sei=Ueda
en-aut-mei=Youki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakedaMidori
en-aut-sei=Takeda
en-aut-mei=Midori
kn-aut-name=
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en-aut-name=DansakoHiromichi
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affil-num=1
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Virology II, National Institute of Infectious Disease

affil-num=6
en-affil=
kn-affil=Department of Drug Informatics, Faculty of Pharmaceutical Sciences, Okayama University

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kn-affil=Department of Drug Informatics, Faculty of Pharmaceutical Sciences, Okayama University

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kn-affil=Department of Drug Informatics, Faculty of Pharmaceutical Sciences, Okayama University

affil-num=9
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

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kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=20040930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=インターフェロン刺激応答配列を介したC型肝炎ウイルスコアタンパク質によるインターフェロン誘導遺伝子の示差的活性化
kn-title=Differential activation of interferon-inducible genes by hepatitis C virus core protein mediated by the interferon stimulated response element
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

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kn-affil=岡山大学
END