数字农科院2.0

Ifn-Kappa Suppresses The Replication Of Influenza A Viruses Through The Ifnar-Mapk-Fos-Chd6 Axis

文献类型： 外文期刊

作者： He, YQ; Fu, WH; Cao, KL; He, Q; Ding, XQ; Chen, J; Zhu, LY; Chen, TY; Ding, LF; Yang, Y; Zhu, CS; Yuan, SH; Li, ZJ; Zhao, C; Zhang, XY; Xu, JQ

作者机构：

期刊名称： SCIENCE SIGNALING

ISSN： 1945-0877

年卷期： 2020 年 13 卷 626 期

页码：

收录情况： JCR（2021版）

摘要： Type I interferons (IFNs) are the first line of defense against viral infection. Using a mouse model of influenza A virus infection, we found that IFN-kappa was one of the earliest responding type I IFNs after infection with H9N2, a low-pathogenic avian influenza A virus, whereas this early induction did not occur upon infection with the epidemic-causing H7N9 virus. IFN-kappa efficiently suppressed the replication of various influenza viruses in cultured human lung cells, and chromodomain helicase DNA binding protein 6 (CHD6) was the major effector for the antiviral activity of IFN-kappa, but not for that of IFN-alpha or IFN-beta. The induction of CHD6 required both of the type I IFN receptor subunits IFNAR1 and IFNAR2, the mitogen-activated protein kinase (MAPK) p38, and the transcription factor c-Fos but was independent of signal transducer and activator of transcription 1 (STAT1) activity. In addition, we showed that pretreatment with IFN-kappa protected mice from lethal influenza viral challenge. Together, our findings identify an IFN-kappa-specific pathway that constrains influenza A virus and provide evidence that IFN-kappa may have potential as a preventative and therapeutic agent against influenza A virus.

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