| Project/Area Number |
25860350
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Virology
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| Research Institution | Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
FUJII Ken 公益財団法人東京都医学総合研究所, ゲノム医科学研究分野, 主任研究員 (10580201)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | エンテロウイルス / 神経病原性 / 神経指向性 / 自然免疫 / マウスモデル / エンテロウイルス71 |
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| Outline of Final Research Achievements |
Enterovirus 71 (EV71) is one of causative agents of hand-foot-mouth disease (HFMD). In EV71 associated HFMD, severe or fatal neurological complications were reported. However, pathogenesis of EV71 is remains unknown. Recently, we generated human SCARB2 transgenic (hSCARB2-Tg) mice model. Here, to understand tropism of EV71, we focused on host innate immune systems. Type I IFN receptor knockout (AR1KO) hSCARB2-Tg mice are highly susceptible to EV71 infection. Viral titers in non-CNS of hSCARB2-Tg-AR1KO mice are higher than that of hSCARB2-Tg wild type mice, suggesting that type I IFN is important for control of EV71 infection in non-CNS. Furthermore, we analyzed features in RNA sensor knockout hSCARB2-Tg mice (MDA5KO, TLR3KO and TLR7KO). The hSCARB2-Tg-TLR7KO mice are slightly susceptible to EV71. EV71 seems to be able to replicate more effectively in the CNS of TLR3 deficient mice. Based on these data, we speculate that both TLR3 and TLR7 may affect EV71 infection in hSCARB2-Tg mice.
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