期刊
IMMUNITY
卷 42, 期 1, 页码 123-132出版社
CELL PRESS
DOI: 10.1016/j.immuni.2014.12.016
关键词
-
类别
资金
- Ministry of Health, Labour and Welfare of Japan
- Ministry of Education, Culture, Sports, Science and Technology of Japan [25253030, 25115502, 23112701, 25870015]
- Kato Memorial Bioscience Foundation
- Yasuda Medical Foundation
- Takeda Science Foundation
- Waksman Foundation of Japan
- IRYO HOJIN SHADAN JIKOKAI
- Grants-in-Aid for Scientific Research [25115502, 25253030, 25114712, 26893001, 24390117, 26102747, 25870015] Funding Source: KAKEN
Host innate recognition triggers key immune responses for viral elimination. The sensing mechanism of hepatitis B virus (HBV), a DNA virus, and the subsequent downstream signaling events remain to be fully clarified. Here we found that type III but not type I interferons are predominantly induced in human primary hepatocytes in response to HBV infection, through retinoic acid-inducible gene-I (RIG-I)-mediated sensing of the 5'-epsilon region of HBV pregenomic RNA. In addition, RIG-I could also counteract the interaction of HBV polymerase (P protein) with the 5'-epsilon region in an RNA-binding dependent manner, which consistently suppressed viral replication. Liposome-mediated delivery and vector-based expression of this e region-derived RNA in liver abolished the HBV replication in human hepatocyte-chimeric mice. These findings identify an innate-recognition mechanism by which RIG-I dually functions as an HBV sensor activating innate signaling and to counteract viral polymerase in human hepatocytes.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据