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2017 Fiscal Year Final Research Report

Analysis and therapeutic targeting of molecular mechanisms by which hepatitis B virus evade the host innate immune response

Research Project

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Project/Area Number 15K09016
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Gastroenterology
Research InstitutionNagoya City University

Principal Investigator

Hamada-Tsutsumi Susumu (浜田進)  名古屋市立大学, 大学院医学研究科, 研究員 (30367693)

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
KeywordsB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
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.

Free Research Field

ウイルス学、免疫学

URL: 

Published: 2019-03-29  

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