期刊
MEDIATORS OF INFLAMMATION
卷 2015, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2015/716315
关键词
-
资金
- National Science and Technology Major Project of the Ministry of Science and Technology of China [2009ZX10004-312]
- National Natural Science Foundation of China [81271885]
It has been reported that IFN-lambda s inhibit HCV replication in vitro. But the mechanisms of how IL-28A conducts antiviral activity and the functions of IL-28A-induced ISGs (IFN-stimulated genes) are not fully understood. In this study, we found that IL-28A has the antiviral effect on HCV life cycle including viral replication, assembly, and release. IL-28A and IFN-alpha synergistically inhibit virus replication. EPSTI1 (epithelial-stromal interaction 1), one of IL-28A-induced ISGs, plays a vital role in IL-28A-mediated antiviral activity. Furthermore, forced expression of EPSTI1 effectively inhibits HCV replication in the absence of interferon treatment, and knockdown of EPSTI1 contributes to viral enhancement. EPSTI1 can activate PKR promoter and induce several PKR-dependent genes, including IFN-beta, IFIT1, OAS1, and RNase L, which is responsible for EPSTI1-mediated antiviral activity.
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