<link rel="stylesheet" href="styles.cf390c6bfbe7555f.css">

學術出版;;Publications

Permanent URI for this communityhdl:11536/1

收集所有交通大學研究人員與學生個人或團體所發表之各項學術著作，涵蓋期刊論文、教師專書、學位論文等項。;;Collections of Publications of NCTU Researchers and Students Like Journal Papers and Thesis.

Browse

🏛️國立陽明交通大學機構典藏

Access type: Open accessSubject: search.filters.subject.HCV

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    Item type:Item,
    Anti-HCV activities of selective polyunsaturated fatty acids
    (2004-05-21)
    Leu, GZ
    ;
    Lin, TY
    ;
    Hsu, JTA
    ;
    生物科技學系
    ;
    Department of Biological Science and Technology
    HCV infection can lead to chronic infectious hepatitis disease with serious sequelae. Interferon-alpha, or its PEGylated form, plus ribavirin is the only treatment option to combat HCV. Alternative and more effective therapy is needed due to the severe side effects and unsatisfactory curing rate of the current therapy. In this study, we found that several polyunsaturated fatty acids (PUFAs) including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA) are able to exert anti-HCV activities using an HCV subgenomic RNA replicon system. The EC50 (50% effective concentration to inhibit HCV replication) of AA was 4 muM that falls in the range of physiologically relevant concentration. At 100 muM, alpha-linolenic acid, gamma-linolenic, and linoleic acid only reduced HCV RNA levels slightly and saturated fatty acids including oleic acid, myristic acid, palmitic acid, and steric acid had no inhibitory activities toward HCV replication. When AA was combined with IFN-alpha, strong synergistic anti-HCV effect was observed as revealed by an isobologram analysis. It will be important to determine whether PUFAs can provide synergistic antiviral effects when given as food supplements during IFN-based anti-HCV therapy. Further elucidation of the exact anti-HCV mechanism caused by AA, DHA, and EPA may lead to the development of agents with potent activity against HCV or related viruses. (C) 2004 Elsevier Inc. All rights reserved.
  • Thumbnail Image
    Item type:Item,
    Let-7b is a novel regulator of hepatitis C virus replication
    (2012-08-01)
    Cheng, Ju-Chien
    ;
    Yeh, Yung-Ju
    ;
    Tseng, Ching-Ping
    ;
    Hsu, Sheng-Da
    ;
    Chang, Yu-Ling
    "The non-coding microRNA (miRNA) is involved in the regulation of hepatitis C virus (HCV) infection and offers an alternative target for developing anti-HCV agent. In this study, we aim to identify novel cellular miRNAs that directly target the HCV genome with anti-HCV therapeutic potential. Bioinformatic analyses were performed to unveil liver-abundant miRNAs with predicted target sequences on HCV genome. Various cell-based systems confirmed that let-7b plays a negative role in HCV expression. In particular, let-7b suppressed HCV replicon activity and down-regulated HCV accumulation leading to reduced infectivity of HCVcc. Mutational analysis identified let-7b binding sites at the coding sequences of NS5B and 5'-UTR of HCV genome that were conserved among various HCV genotypes. We further demonstrated that the underlying mechanism for let-7b-mediated suppression of HCV RNA accumulation was not dependent on inhibition of HCV translation. Let-7b and IFN alpha-2a also elicited a synergistic inhibitory effect on HCV infection. Together, let-7b represents a novel cellular miRNA that targets the HCV genome and elicits anti-HCV activity. This study thereby sheds new insight into understanding the role of host miRNAs in HCV pathogenesis and to developing a potential anti-HCV therapeutic strategy."