| Project/Area Number |
18F18098
|
|---|
| Research Category |
Grant-in-Aid for JSPS Fellows
|
| Allocation Type | Single-year Grants |
|---|
| Section | 外国 |
|---|
| Research Field |
Virology
|
|---|
| Research Institution | National Institute of Infectious Diseases |
|---|
Principal Investigator |
アリ フセインハッサン 国立感染症研究所, ウイルス第二部, 主任研究官 (00523515)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
IBRAHIM MARWA 国立感染症研究所, ウイルス第二部第三室, 外国人特別研究員
|
|---|
| Project Period (FY) |
2018-10-12 – 2021-03-31
|
| Project Status |
Completed (Fiscal Year 2020)
|
| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2020: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2019: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2018: ¥600,000 (Direct Cost: ¥600,000)
|
|---|
| Keywords | HBV / pgRNA / MafF / RNA degradation / IL-1b / HBV-pgRNA / HBV-RNA / Degradation / virus host interaction / Transcription |
|---|
| Outline of Annual Research Achievements |
Hepatitis B Virus (HBV) is a stealth virus that exhibits only minimal induction of the interferon system that is required for both innate and adaptive immune responses. However, 90% of acutely infected adults can clear the virus, suggesting the presence of additional mechanisms that facilitate viral clearance. Marwa identified Maf bZIP transcription factor F (MafF) to promote host defense against infection with HBV. MafF was found to control HBV-pgRNA levels. Her data showed that silencing of MafF led to 6-fold increase in luciferase activity after HBV/NL infection, induced HBV-pgRNA levels, HBV replication, and the expression of HBV core protein expressed from HBV-pgRNA. Overexpression of MafF reduced HBV core promoter transcriptional activity, which was relieved upon mutating the putative MafF binding region. Marwa found that MafF is induced by famous inflammatory cytokines IL-1b and TNF-a. Analyzing the data from human hepatocytes chimeric mouse infected in-vivo with HBV, or single cell data from primary hepatocytes infected in-vitro with HBV; she found that MafF levels were induced after HBV infection, confirming the induction of MafF levels in response to HBV infection. The anti-viral effect of MafF was also extended to EBV, where MAfF suppressed genes required for activation of EBV infection (BZLF1 gene).
|
| Research Progress Status |
令和2年度が最終年度であるため、記入しない。
|
| Strategy for Future Research Activity |
令和2年度が最終年度であるため、記入しない。
|
