| Project/Area Number |
60480171
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Virology
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| Research Institution | Niigata University, |
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Principal Investigator |
ICHIHASHI Yasuo Associate Professor, Niigata University School of Medicine, 医学部, 助教授 (80027317)
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| Co-Investigator(Kenkyū-buntansha) |
OIE Masayasu Assistant, Niigata University School of Medicine, 医学部, 助手 (70108017)
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| Project Period (FY) |
1985 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1987: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1986: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1985: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Vaccinia virus / Infection mechanism of verus / 細胞膜プロテアーゼ / 細胞内侵入機構 / モノクローナル抗体 / ウイルスレセプター |
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| Research Abstract |
Adsorption and penetration steps of virus infection determine viral tropism and disease patterns. The adsorption is achieved by interaction between viral ligand and host cell receptor, and penetration occurrs through fusion between viral and cellular membranes following adsorption or after phagocytosed. However, little is known about the molecular events of these processes.
We analyzed the phenomena related to the vaccinia virus infection that the infectivity of vaccinia virus can be increased by in vitro treatment of the virus with proteolytic enzyme or with phosphatidylserine. These activation of the virus infectivity seem to occur also in vatural infection process on host cell surface. We made several neutralizing monoclonal antibodies (MAb) which are specifically reactive against viral surface proteins. All of the MAbs did not significantly affect on absorptive efficiency of the virus to the cell surface, but showed differential neutralizing titers according to the activated state of the virus. The reactivity of the MAbs against the virus before and after the ativating treatments revealed that the proteolytic treatment cleaves VP54K to TVP41K, and PS-treatment changes epitope structure of VP3jK. An anti-idiotypic antibody against anti-VP3iK and/or VP32K was found to mediate activation of the virus through interaction with 32K Vero cell receptor. We concluded that vaccinia virus penetration took place through multi-step reaction. Viral surface proteins exist in a disulfide-linked complex, and each protein performs specific reaction of the process.
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