北海道大学 · 医学
Naoya Sakamoto教授の研究室では、ウイルス感染の回避機構に注目し、特にヘパチティスCウイルス（HCV）が宿主のインナート免疫応答をどのように回避するかを分子レベルで解明しています。NS5B や NS4B といったウイルスタンパク質が、STING や GBP-1 といった宿主因子と相互作用することで、インターフェロン応答を阻害するメカニズムを解明しています。また、リボゾームを用いたウイルスRNAの標的分解や、ウイルス複製の恒常化が宿主のインターフェロン応答を抑制する仕組みについても研究を展開しています。
Figures are computed from collected data and may differ slightly.
Binding of the HCV-NS5B protein to GBP-1 countered the antiviral effect by inhibition of its GTPase activity. These mechanisms may contribute to resistance to innate, IFN-mediated antiviral defense and to the clinical persistence of HCV infection.
NS4B suppresses RIG-I-mediated IFN-β production signaling through a direct protein interaction with STING. Disruption of that interaction may restore cellular antiviral responses and may constitute a novel therapeutic strategy for the eradication of HCV.
To determine the effects of hammerhead ribozymes against hepatitis C virus (HCV) RNA on viral protein translation, a luciferase reporter gene vector, pCMV/T7-NCRCdelta-luc, was constructed containing the 5'-noncoding region (5'-NCR) and part of the core region of HCV. Four ribozymes, Rz1-Rz4, were designed to cleave at nucleotide positions 136-160, 313-337, 496-520, and 373-388, respectively. Each ribozyme cleaved the target RNA at expected positions under cell-free conditions. Rz2 and Rz4 signi
Cellular antiviral responses are mediated partly by the expression of interferon-stimulated genes, triggered by viral genomes, their transcripts and replicative intermediates. Persistent replication of a hepatitis C virus (HCV) replicon suggests that the replicon does not elicit cellular innate antiviral responses. In the present study, we investigated regulatory factors of the interferon-mediated antiviral system in cells expressing an HCV replicon. Luciferase reporter assays revealed that the
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