| Project/Area Number |
16K08260
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
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| Research Collaborator |
Shirasago Yoshitaka
Shimizu Yoshimi
Ogawa Motohiko
Suzuki Takeru
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | C型肝炎ウイルス / 受容体 / 宿主細胞 / モノクローナル抗体 / HCV / ウイルス / ノックアウト細胞 |
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| Outline of Final Research Achievements |
We have developed many kinds of useful tools for analyzing hepatitis C virus (HCV) entry mechanisms, such as viral receptor-defective cell lines, anti-viral receptor monoclonal antibodies, and highly infectious HCV strains. In this project, using these tools, we isolated HCV-JFH1 sub-strains having different host receptor-dependency. We also showed that one isolated sub-strain uses new host molecule as its entry receptor. It seemed that these phenotypes of sub-strains can be acquired by only one amino acid mutation.
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| Academic Significance and Societal Importance of the Research Achievements |
特定のC型肝炎ウイルス（HCV）受容体に非依存性を獲得したHCV変異亜株が(比較的簡便に)分離されることを示し、そのメカニズムの一端を明らかにした。以上の成果は、宿主-ウイルス間の攻防の分子基盤の進化を考える上で、学術的意義は大きいと考えている。また、受容体の選択性が変わることで、肝臓以外に感染する能力を獲得しうることから、依然として不明の点の多い、HCVによる肝外病変の発症メカニズムを考えるヒントとなる可能性があり、医学的な見地からも意義があるかもしれない。
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