2020 Fiscal Year Final Research Report
Machinery for hepatitis B virus entry regulated by host protein kinase
| Project/Area Number |
19K16672
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 49060:Virology-related
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2019-04-01 – 2021-03-31
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| Keywords | HBV / プロテインキナーゼ / EGFR |
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| Outline of Final Research Achievements |
Machinery for entry of hepatitis B virus (HBV) into the host cells have been largely unknown. Here, we reported epidermal growth factor receptor (EGFR) as essential host factor for HBV entry after attachment to sodium taurocholate co-transporting polypeptide (NTCP), known as HBV host receptor, on the plasma membrane. EGFR triggered HBV internalization thought binding to NTCP. Future studies revealed that role of EGFR on HBV entry was not only inducing viral internalization, but also regulating the trafficking of HBV to late endosome for functional infection. These results are useful for understanding the mechanism of HBV infection as well as establishment of novel anti-HBV agents.
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| Free Research Field |
ウイルス学
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| Academic Significance and Societal Importance of the Research Achievements |
本研究課題により、長年明らかでなかったHBVの細胞内侵入機構の一端を明らかにした。EGFRはHBV感染に必須な宿主因子であり、その感染制御機構を同定した。EGFRはこれまでに抗がん剤の標的として着目されてきたことにより、多くの阻害剤が報告されており、これらのうち少なくともゲフィチニブはEGFRの機能を阻害することでHBV感染を減少させることを細胞培養レベルで明らかにした。本研究で得た知見はHBV感染分子機構の理解を推し進めたのみならず、新しいHBV感染治療戦略を提案するもので、 EGFRが新規HBV治療薬の標的となり得る可能性を示唆した。
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