| Project/Area Number |
62580032
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory animal science
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| Research Institution | University of Tsukuba |
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Principal Investigator |
YAGAMI Kenichi Univ. of Tsukuba, Inst. of Basic Med., Associate Prof., 基礎医学系, 助教授 (40166476)
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| Co-Investigator(Kenkyū-buntansha) |
SUGIYAMA Yoshihiro Univ. of Tsukuba, Inst. of Basic Med., Assist.Prof., 基礎医学系, 講師 (10187685)
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| Project Period (FY) |
1987 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1989: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1988: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | Hemagglutinating encephalomyelitis virus / Coronavirus / mice / Age-dependent resistance / Immunosuppression / Immuno-histochemistry / 酵素抗体法 / 年令依存抵抗性 / 免疫機能不全マウス / 赤血球凝集性脳脊髄炎ウィルス |
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| Research Abstract |
The age-dependent resistance of mice to fatal infection with hemagglutinating encephalomyelitis virus (HEV) was investigated. MB-67N strain of HEV caused acute fatal infection of central nervous system(CNS). This virus had neurotropism, and propagated in CNS such as nerve cells of cerebral cortex and Purkinje's cells in cerebellum. In intranasal(in) infection, it was suggested that the virus spread from primary sites of viral replication via offactory nerve to the CNS. Although there was no difference between these infectious process of adult and newborn, age-dependent resistance to fatal encephalomyelitis was found. The resistance of newborn mice was increased progressively accompanied with age, and of age-dependency was more remarkable in intracerebral(ic) than in infection. The resistance in adult mice was influenced with genetic background of mice, but not reduced in immunodeficient (T-, B-, and NK-deficient) and immunosuppressive (prednisolone- and cyclophosphamide-treated)mice. It was suggested that the age-dependent resistance of mice to fatal HEV infection had little relation with maturation of immunological function in viral spread from peripheral site to CNS, but influenced with viral replication on nerve cells in CNS. The factors rented with age-dependent resistance may be production of the interferon in CNS or differentiation and maturation of nerve cells in cerebral cortex.
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