| Project/Area Number |
61570381
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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 |
Neurology
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
TSUKAMOTO Tetsuro Department of Neurology, Tohoku Uni. School of Medicine, 医学部付属病院, 助手 (20171978)
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| Co-Investigator(Kenkyū-buntansha) |
TAKASE Sadao Dept. of Neurology, Tohoku Uni. School of Medicine, 医学部脳研神経内科, 助教授 (60004983)
SEKIZAWA Tsuyoshi Dept. of Neurology, Tohoku Uni. School of Medicine, 医学部付属病院神経内科, 助手 (50150264)
YOSHIE Osamu Dept. of Bacteriology, Tohoku Uni. School of Medicine, 医学部細菌学, 助手 (10166910)
IWASAKI Yuzo Dept. of Neurol. Sci., Tohoku Univ. School of Medicine, 医学部病態神経学, 教授 (00142927)
HIRANO Norio Dept. of Vet. Microbiol., Iwate University, 農学部・家畜微生物, 助教授 (40092308)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1986: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Coronavirus / Chronic vacuolar degeneration / 脳炎モデル / vacuolar degeneraition |
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| Research Abstract |
Neuropathogenicity of a mutant of mouse hepatitis virus (MHV), JHMcc which was derived from DBT cell cultures persistently infected with MHV-JHM was studied in mice. Four-week-old ICR mice were inoculated intracerebrally or intranasally with 10^6 PFU of JHMcc virus. Five days after intracerebral inoculation about 20% of mice began to develop hindlimb paralysis.The viral titers in the brain and spinal cord were 10^6PFU/0.2g ata peak 4 or 5 days after infection, then decreased gradually and no virus was rescued any more after 14 days postinoculation. Pathologically, the most remarkable finding was marked vacuolar changes in the brainstem and spinal cord white matter in addition to inflammatory cell infiltrations in the meninges and around the small vessels in the brain, neuronophagia and glial nodules. These changes progressed in size and number even after disapperance of infectious virus and viral antigens. After intranasal infection the viral antigens seemed to appear through the olfactory system and finally reached in the brainstem and spinal cord neurons. An electromicroscopic analysis revealed that the vacuolar changes weredue to marked myelin splitting and intralamellar edema and in part to intraneurite vacuolation. They could not be prevented with cyclofosphamide treatment or in nude mice. JHMcc virus dose not cause demyelination in mice, but characteristic vacuolar changes which resemble pathologically vacuolar myelopathy in AIDS or spinal cord degeneration in HAM. This JHMcc virus infection model could be useful to elucidate the mechanism of vacuolar degeneration associatedwith some viral infections.
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