期刊
ANTIVIRAL RESEARCH
卷 85, 期 3, 页码 504-511出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.antiviral.2009.12.007
关键词
IFN-stimulated gene 15; Japanese encephalitis virus; IRF-3; JAK2; STAT1
资金
- National Science Council (Taiwan)
- China Medical University [NSC96-2320-B-039-008-MY3, CMU97-140, CMU97-CMC-020]
IFN-stimulated gene 15 (ISG15), an ubiquitin-like protein, is rapidly induced by IFN-alpha/beta, 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-beta, 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. Crown Copyright (C) 2009 Published by Elsevier B.V. All rights reserved.
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