2021 Fiscal Year Final Research Report
Biological Significance of Latent Viral Infection
| Project Area | Neo-virology: the raison d'etre of viruses |
|---|
| Project/Area Number |
16H06433
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
|
| Allocation Type | Single-year Grants |
|---|
| Review Section |
Biological Sciences
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2016-06-30 – 2021-03-31
|
| Keywords | ウイルス / HSV / 潜伏感染 / 共生維持機構 / 免疫回避機構 / 感染享受 |
|---|
| 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.
|
| Free Research Field |
ウイルス学
|
| Academic Significance and Societal Importance of the Research Achievements |
HSV感染制御に重要な宿主免疫応答および効率的なウイルス増殖のためにウイルス因子によってそれらを回避する機序を理解することや、HSVが細胞内で如何にして増殖するかを理解することは、ウイルスと宿主との共生維持機構を明らかにするだけでなく、抗HSV剤やワクチン開発の基盤情報をなり得る。
|
