| Budget Amount *help |
¥140,920,000 (Direct Cost: ¥108,400,000、Indirect Cost: ¥32,520,000)
Fiscal Year 2020: ¥25,740,000 (Direct Cost: ¥19,800,000、Indirect Cost: ¥5,940,000)
Fiscal Year 2019: ¥26,130,000 (Direct Cost: ¥20,100,000、Indirect Cost: ¥6,030,000)
Fiscal Year 2018: ¥25,740,000 (Direct Cost: ¥19,800,000、Indirect Cost: ¥5,940,000)
Fiscal Year 2017: ¥26,130,000 (Direct Cost: ¥20,100,000、Indirect Cost: ¥6,030,000)
Fiscal Year 2016: ¥37,180,000 (Direct Cost: ¥28,600,000、Indirect Cost: ¥8,580,000)
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| Outline of Final Research Achievements |
The mechanism of maintaining symbiosis between herpes simplex virus (HSV) and the host obtained the following results. (i) HSV-encoded protein kinase UL13 suppresses the response of cytotoxic T cells. (ii) HSV virion protein VP22 rapidly and efficiently inhibits the activation of the inflammasome. (iii) HSV-1 expropriates the ESCRT-III machinery in infected cells for scission of the inner nuclear membrane (INM) to produce vesicles containing progeny virus nucleocapsids. (iv) Host mTORC2 controls TLR3, a sensor of double-stranded RNA, and suppresses herpesvirus encephalitis. (v) The lattice formation of the nuclear egress complex (NEC) hexamer has an important role in HSV-1 replication.
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