Analysis and therapeutic targeting of molecular mechanisms by which hepatitis B virus evade the host innate immune response
Project/Area Number |
15K09016
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | Nagoya City University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
Tanaka Yasuhito 名古屋市立大学, 大学院医学研究科, 教授 (90336694)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | B型肝炎ウイルス(HBV) / 自然免疫 / 核酸センサー / インターフェロン / HBV / 自然免疫応答 / Type III インターフェロン / HBs抗原 / B型肝炎ウイルス / インターフェロンλ |
Outline of Final Research Achievements |
In this study, we investigated the impact of HBV infection on the induction of type I and type III interferon (IFN) by stimulation of intracellular nucleic acid sensors in the hepatocytes. A HBV-permissive cell line, Hep G2-NTCP, was infected with HBV and transfected with double-strand RNA to activate nucleic acid sensors. Interestingly the induction of type I/III IFNs was significantly suppressed in the HBV-infected cells. Oh the other hand, the amounts of intracellular HBV mRNAs and extracellular viral antigen were greatly reduced in the double-strand RNA-treated group in the absence of IFNs, Thus, the activation of nucleic acid sensors induces uncharacterized antiviral pathways independent of conventional type I/III interferon signaling.
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Report
(4 results)
Research Products
(6 results)