Suppression of the IRF-3 signaling pathway by the sfRNA of Japanese encephalitis virus is TANK-binding kinase-1 independent

• Main Authors: Shu-Fan Liou, 劉書帆
• Other Authors: Ruey-Yi Chang
• Format: Others
• Published: 2012
• Online Access: http://ndltd.ncl.edu.tw/handle/5y5ja9

碩士 === 國立東華大學 === 生命科學系 === 100 === Noncoding RNA (ncRNA) plays a critical role in modulating various stages of viral life cycle. Abundant ncRNA (named sfRNA), representing a highly conserved region of the 3’-untranslated region (UTR) of Japanese encephalitis virus (JEV), accumulated in JEV-infected cells. Previous work in our laboratory demonstrated that transfecting sfRNA into JEV-infected cells inhibited phosphorylation of interferon regulatory factor-3 (IRF-3), blocked roughly 30% of IRF-3 nuclear translocation, and reduced interferon-β by 50%. In this study, transfection of sfRNA had no effect on TANK-binding kinase 1 (TBK1) protein expression or its phosphorylation. Furthermore, the sfRNA binds to viral NS5 protein, but not to the IRF-3 or RIG-I molecules as demonstrated by ribonucleoportein co-immunoprecipitated (RIP) assay. RNAi knockdown of TBK1 resulted in enhancement of IRF-3 phosphorylation and reduction of virus particles. Taken together, these results indicated that suppression of the IRF-3 signaling pathway by the sfRNA is TBK1 independent. JEV induced anti-viral responses may be different from other viruses. Further research is needed to better understand the detailed evasion mechanisms mediated by the sfRNA in host innate immune responses.