| Project/Area Number |
22590421
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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 |
Virology
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
OHARA Yoshiro 金沢医科大学, 医学部, 教授 (50203914)
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| Co-Investigator(Kenkyū-buntansha) |
HIMEDA Toshiki 金沢医科大学, 医学部, 講師 (80340008)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 病原性 / タイラーウイルス / 持続感染 / L蛋白 / L*蛋白 / アポトーシス / インターフェロン / ウイルス / 脳・神経 |
|---|
| Research Abstract |
Theiler's murine encephalomyelitis virus (TMEV)-induced demyelination is the representative of virus-induced demyelination and serves as an excellent animal model for multiple sclerosis because of the resembling pathological features. Twonon-structural viral proteins, leader (L) and L*, are thought to play an important role in TMEV biological activities.In this study, it was demonstrated that L increases the number of apoptotic cells while it suppresses the IFN response of host cells. Furthermore, it was demonstrated that L* inhibits the apoptotic cell death induced by L. In addition, L* was demonstrated to be localized to mitochondria. These results suggest that L* may inhibit the intrinsic apoptosis induced by L through the localization to mitochondria.The present studies suggest that the L and L* regulate the apoptosis during viral infection and contribute to TMEV subgroup-specific biological activities.
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