Cell Mol Immunol. 2018 Mar 9. doi: 10.1038/s41423-018-0006-2. [Epub ahead of print]
Type III interferon-induced CBFβ inhibits HBV replication by hijacking HBx.
Xu F1, Song H1, Xiao Q2, Li N3, Zhang H4, Cheng G1, 5,6, Tan G7.
Author information
1
Department of Immunology, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin, 130061, China.
2
Department of Nephrology, The First Hospital, Jilin University, Changchun, Jilin, 130021, China.
3
Department of Obstetrics, The First Hospital of Jilin University, Changchun, Jilin, 130021, China.
4
Phase I Clinical Research Center, The First Hospital of Jilin University, Jilin, 130021, China.
5
Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, 90095, USA.
6
Center of Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100005; Suzhou Institute of Systems Medicine, Suzhou, Jiangsu, 215123, China.
7
Department of Immunology, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin, 130061, China. [email protected].
Abstract
Hepatitis B virus (HBV) and its associated seamless studies of worldwide wellbeing threat of worldwide. yet, there is no impactful approach for clinical treatment of hepatitis B patients. developing, better a better understanding of the interactions between HBV and its host HBV infection has been reported to induce type-III but not type-I or type-II interferon (IFN). In this study, we identified CBFβ, an HIV enhancer, as an HBV restriction factor that is specifically induced by type-III IFN in the early stages of HBV infection. Type-III IFN-induced IL-10 played an important role in the production of CBFβ. Interestingly, the interaction between CBFβ- and HBV-encoded regulatory protein X (HBx) enhanced the stability of CBFβ. , but notably blocked HBx-mediated promotion of HBV replication. CBFβ expression was lower in HBV patients than in healthy persons, and the addition of serum from HBV patients inhibited CBFβ expression in HepG2 cells. On the In contrast, HBV via HBsAg inhibited type-III IFN-induced CBFβ expression and decreased the anti-HBV activity of type-III IFN, suggesting that HBV inhibits antiviral interferon-stimulated gene (ISG) expression and induces IFN resistance. Collectively, our values represents That type-III IFN-triggered and IL-10-induced CBFβ are are factors for inhibiting HBV replication, and the HBx-CBFβ-HBsAg axis reveals a new molecular mechanism of interaction between HBV and its hosts.
PMID:29523836DOI:10.1038/s41423-018-0006-2 作者: StephenW 时间: 2018-3-11 21:26