| Project/Area Number |
07457075
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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 | Niigata University |
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Principal Investigator |
ICHIHASHI Yasuo Faculty of Medicine, Niigata University Associate Professor, 医学部, 助教授 (80027317)
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| Co-Investigator(Kenkyū-buntansha) |
OIE Masayasu Faculty of Medicine, Niigata University Assistant, 医学部, 助手 (70108017)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Infection Mechanism / Neutralization Mechanism / Membrane Fusion / Vaccinia Virus / Resistanay to Antibody / ワクケニアウイルス / ウイルス中和機構 / ワクチニアウイルス / ウイルスの抗体抵抗性 |
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| Research Abstract |
The vaccinia virus infection efficiency elevates by treatment with protease, and similar high infecting efficiency is observed in HA^- mutants. It suggested that the infection process is affected by interaction between HA and penetration protein. The penetration protein of vaccinia virus (VP23-29K : L1R encoded myristylated protein) is neutralized by 2D5mAb, but that of mousepox virus is resistant. Hybrid viruses that have (VAC VP23-29K/MPV HA) or (MPV VP23-29K /VAC HA) was produced. The analysis of the infectivity and sensitivity to 2D5mAb indicated that the VP23-29K interacts with HA and changes the epitope. It suggested that the interaction is a mechanism to escape neutralization.
The VP23-29K has amino acid sequence resembled to that of TNF active site region (hTNF-a 83-99) at the N-terminal, and induced apoptosis. The apoptosis was blocked by additional treatment of the cells with the UV-inactivated virus and also by super infection with the virus. The virus-cell membrane fusion by the VP23-29K seems to trigger apoptotic cascade of the host cells by interaction with the TNF receptor. Viral serpins blocked the process to compensate for the side effect of the penetration. Possibly, the early step of the apoptosis produce cell membrane conditions preferable to the virus infection. However, the TNF and anti-TNF did not inhibit infection of the virus.
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