| Project/Area Number |
17H06728
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Veterinary medical science
|
|---|
| Research Institution | Gifu University |
|---|
Principal Investigator |
Okada Kazuma 岐阜大学, 応用生物科学部, 研究員 (50806354)
|
|---|
| Project Period (FY) |
2017-08-25 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| Keywords | 狂犬病ウイルス / 自然免疫 / 神経細胞 / 筋肉細胞 / 獣医学 / ウイルス学 / 免疫学 / 人獣共通感染症学 |
|---|
| Outline of Final Research Achievements |
It has been showed that rabies virus (RABV) P protein isoforms (P1 and tPs) are known as viral antagonists of interferon (IFN), which play the key role to mediate the host innate immune responses. In our previous study, RABV requires P1 and P2-5 for viral replication in muscle tissues, while it requires only P1 for the replication in neural tissues (Okada et al, J. Virol., 2016), leading to the hypothesis that different isoforms contribute to the inhibition of IFN induction in neural and muscle cells. This study investigated this hypothesis and indicated that P1 is sufficient to inhibit IFN induction in neural cells infected with RABV, whereas P2-5 are also required to suppress the induction in infected muscle cells.
|
| Academic Significance and Societal Importance of the Research Achievements |
狂犬病ウイルスは筋肉細胞における増殖により神経系に侵入した後、中枢神経系内の神経細胞において増殖し、その病態を形成する。病態形成において狂犬病ウイルスが異なる細胞種に感染し増殖する機序の一端を、本研究の成果により明らかにすることができた。この成果は、今後、狂犬病ウイルスが神経系に侵入するのを阻害する発症阻害薬、またより効果的かつ安全なワクチン開発の研究において必要となり得る情報の蓄積に貢献した。
|
