| Project/Area Number |
12670609
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
KIKUCHI Hitoshi Dept. of Neurology, KYUSHU UNIVERSITY, Instructor, 医学部・附属病院, 助手 (60322765)
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| Co-Investigator(Kenkyū-buntansha) |
MURAI Hiroyuki Dept. of Neurology, KYUSHU UNIVERSITY, Instructor, 医学部・附属病院, 助手 (80325464)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | Theiler's murine encephalomyelitis virus / Multiple sclerosis / L* / Demyelination / Persistent infection / 脱髄 / 持続感染 |
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| Research Abstract |
Theiler's murine encephalomyelitis virus (TMEV) is divided into two subgroups on the basis of their biological activities. DA and other members of the TO subgroups cause persistent infection in CNS of mice followed by inflammatory demyelination and serve as an experimental model of multiple sclerosis (MS). In contrast, GDVII subgroups produce an acute fatal neuronal disease and kill mice within 7 days. The pathomechanism of persistent infection and demyelination caused by TMEV remain uncertain. Recently, a novel protein called L* that is synthesized by demyelinating strains of TMEV was reported to play an important role in the persistent infection and demyelination. GDVII subgroups do not synthesize this protein. We made mutant GDVII viruses that could synthesize L*. One of them (GDstemL*AUG) could persistently infect in mice but did not cause demyelination. This result suggests that the responsible regions for demyelination and persistent infection are different. We are now making and evaluating chimera constructs between GDstemL*AUG and DA capsids to determine the critical region for demyelination.
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