IFN-kappa suppresses the replication of influenza A viruses through the IFNAR-MAPK-Fos-CHD6 axis

文献类型： 外文期刊

第一作者： He, Yongquan

作者： He, Yongquan;Fu, Weihui;Cao, Kangli;He, Qian;Ding, Xiangqing;Chen, Jian;Zhu, Lingyan;Chen, Tianyue;Ding, Longfei;Yang, Yu;Zhu, Cuisong;Yuan, Songhua;Zhao, Chen;Zhang, Xiaoyan;Xu, Jianqing;He, Yongquan;Fu, Weihui;Cao, Kangli;He, Qian;Ding, Xiangqing;Chen, Jian;Zhu, Lingyan;Chen, Tianyue;Ding, Longfei;Yang, Yu;Zhu, Cuisong;Yuan, Songhua;Zhao, Chen;Zhang, Xiaoyan;Xu, Jianqing;Li, Zejun;Zhang, Xiaoyan;Xu, Jianqing

作者机构：

期刊名称：SCIENCE SIGNALING （ 影响因子：8.192； 五年影响因子：8.384 ）

ISSN： 1945-0877

年卷期： 2020 年 13 卷 626 期

页码：

收录情况： SCI

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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