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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16410


    Title: ISG15 over-expression inhibits replication of the Japanese encephalitis virus in human medulloblastoma cells
    Authors: 林振文;LIN, CHENG-WEN
    Contributors: 生物科技學系
    Keywords: IFN-stimulated gene 15;Japanese encephalitis virus;IRF-3;JAK2;STAT1
    Date: 2010-03
    Issue Date: 2012-11-23 17:12:42 (UTC+8)
    Abstract: IFN-stimulated gene 15 (ISG15), an ubiquitin-like protein, is rapidly induced by IFN-α/β, and ISG15 conjugation is associated with the antiviral immune response. Japanese encephalitis virus (JEV), a mosquito-borne neurotropic flavivirus, causes severe central nervous system diseases. We investigated the potential anti-JEV effect of ISG15 over-expression. ISG15 over-expression in human medulloblastoma cells significantly reduced the JEV-induced cytopathic effect and inhibited JEV replication by reducing the viral titers and genomes (p < 0.05, Student's t-test); it also increased activation of the interferon stimulatory response element (ISRE)-luciferase cis-acting reporter in JEV-infected cells (p < 0.05, Chi-square test). Furthermore, Western blotting revealed that ISG15 over-expression increased phosphorylation of IRF-3 (Ser396), JAK2 (Tyr1007/1008) and STAT1 (Tyr701 and Ser727) in JEV-infected cells (P < 0.05, Chi-square test). Confocal imaging indicated that nucleus translocation of transcription factor STAT1 occurred in ISG15-over-expressing cells but not in vector control cells post-JEV infection. ISG15 over-expression activated the expression of STAT1-dependent genes including IRF-3, IFN-β, IL-8, PKR and OAS before and post-JEV infection (p = 0.063, Student's t-test). The results enabled elucidation of the molecular mechanism of ISG15 over-expression against JEV, which will be useful for developing a novel treatment to combat JEV infection.
    Relation: ANTIVIRAL RESEARCH
    Appears in Collections:[生物科技學系] 期刊論文

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