| Project/Area Number |
15K19103
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Virology
|
|---|
| Research Institution | Chiba University |
|---|
Principal Investigator |
ONOMOTO KOJI 千葉大学, 真菌医学研究センター, 助教 (10612202)
|
|---|
| Project Period (FY) |
2015-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | ウイルス学 / 自然免疫 / RLR / ストレス応答 / ウィルス |
|---|
| Outline of Final Research Achievements |
RIG-I-like receptors (RLRs), cytoplasmic viral RNA sensors, induce antiviral innate immunity, including production of IFN. In this project, we focused on cellular localization of RLRs and detail mechanism of antiviral stress granules (avSGs), which plays critical role for sensing viral RNA by RLRs to trigger RLRs-mediated antiviral innate immune signals. We found that in Newcastle disease virus (NDV)-infected cells, RIG-I localized in viral replication complex (vRC), consisting of viral proteins and RNAs, at early phase and subsequently in avSGs which contains viral read-through RNAs. Both vRCs and avSGs are important for detecting viral RNAs and primary and secondary production of IFN by RIG-I. We also found several novel candidate proteins that involved RLR-mediated signals among avSG localized proteins. For further study, we will analyze regulatory mechanisms of these candidate proteins and elucidate avSG-mediated RLR signaling.
|
