期刊
SCIENTIFIC REPORTS
卷 6, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep27778
关键词
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资金
- National Science Foundation [31500142, 31370204]
- Natural Science Foundation of Guangdong Province [2014A030310357, 2015A030310130, 2016A030310279]
- China Postdoctoral Science Foundation [2015M572291, 2015M572292]
- Educational Commission of Guangdong Province [2014KQNCX116]
- Science and Technology Project of Guangzhou Municipal Universities [1201420868]
- Science and Technology Planning Project of Guangdong Province [2015A020213005]
- Innovative Research Team of Department of education of Guangdong Province [2014KCXTD015]
Hepatitis C virus (HCV) uses components of the very-low-density lipoprotein (VLDL) pathway for assembly/release. We previously reported that hepatocyte nuclear factor 4 alpha (HNF4 alpha) participates in HCV assembly/release through downstream factors those participate in VLDL assembly/secretion. Cell-death-inducing DFFA-like effector B (CIDEB) is an important regulator of the VLDL pathway. CIDEB is required for entry of HCV particles from cell culture (HCVcc), but the effects of CIDEB on the post-entry steps of the HCV lifecycle are unclear. In the present study, we determined that CIDEB is required for HCV assembly in addition to HCVcc entry. Furthermore, CIDEB interacts with the HCV NS5A protein, and the N terminus of CIDEB and the domain I of NS5A are involved in this interaction. Moreover, CIDEB silencing impairs the association of apolipoprotein E (ApoE) with HCV particles. Interestingly, CIDEB is also required for the post-entry stages of the dengue virus (DENV) life cycle. Collectively, these results indicate that CIDEB is a new host factor that is involved in HCV assembly, presumably by interacting with viral protein, providing new insight into the exploitation of the VLDL regulator CIDEB by HCV.
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