| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2019: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2018: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2017: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
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| Outline of Final Research Achievements |
The development of a novel animal model exhibiting similar receptor specificities in humans is critical to elucidate the mechanism of neuropathogenicity due to EV-A71 infection. In a cynomolgus model, infection with the PSGL-1-binding EV-A71 strain (VP1-145Q) did not induce apparent virus replication and pathogenesis. We then established knock-in mice expressing several human EV-A71 receptors and investigated viral replication and pathogenicity in the mice infected with various EV-A71 strains. However, any viral replication and clinical symptoms were not observed. In this study, we failed to develop an animal model for the PSGL-1-dependent replication and pathogenicity but gained valuable insights to improving animal models for analyzing human receptor specificities against EV-A71.
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