| Project/Area Number |
16H05195
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | Osaka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
荒瀬 尚 大阪大学, 微生物病研究所, 教授 (10261900)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2018: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2017: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2016: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
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| Keywords | ヘルペスウイルス / エントリー / 膜融合（fusion) / ペア型レセプター / 免疫逃避 / 糖鎖修飾 / マラリア病原虫 / 膜融合 / 糖鎖 / マラリア原虫 / トロピズム |
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| Outline of Final Research Achievements |
We identified entry receptors of herpes simplex virus and varicella-zoster virus that are included in human herpesvirus family. These receptors induce the fusion between the viral envelope and host membrane during the viral entry into host cells. Glycosylation of the certain molecules on herpesvirus is required for the virus entry and membrane fusion mediated with the identified receptors. Furthermore, it is elucidated that the tissue, which these viruses preferentially entry (entry tropism), depends on the type of glycans.
Paired receptor family is known to regulate immune cells positively and negatively. We clarified that certain paired receptor family molecules inhibit the entry of human herpesvirus-6 and the other paired receptor family molecule, LILRB1, is utilized for immune evasion by malaria parasites. These results suggested that paired receptor family molecules play an important role in the offense and defense between host and pathogens.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、主にヘルペスウイルスファミリーのウイルス粒子が宿主細胞へ侵入する機構を解析したものである。ウイルスがヒトなどの宿主に感染するためには、宿主の細胞内に侵入しなければならない。細胞侵入のための宿主側の受容体分子や侵入阻害分子、逆に侵入を惹起するウイルス側のエンベロープ分子とそれらの糖鎖修飾を明らかにすることによって、各ヘルペスウイルスファミリーのウイルスが、どの臓器や組織に侵入しやすいかのメカニズムを解明した。本研究の知見は、ウイルス侵入を阻害して、ヘルペスウイルスの感染予防や感染拡大の制御に役立つものと考えられる。
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