The Nucleoprotein and Phosphoprotein of Peste des Petits Ruminants Virus Inhibit Interferons Signaling by Blocking the JAK-STAT Pathway

文献类型： 外文期刊

第一作者： Li, Pengfei

作者： Li, Pengfei;Zhang, Miaotao;Wu, Chunyan;Nan, Yuchen;Li, Pengfei;Zhu, Zixiang;Zhang, Xiangle;Dang, Wen;Li, Linlin;Du, Xiaoli;Liu, Xiangtao;Zheng, Haixue;Xue, Qinghong

作者机构：

关键词： peste des petits ruminants virus; nucleoprotein; phosphoprotein; interferon; JAK; STAT

期刊名称：VIRUSES-BASEL （ 影响因子：5.048； 五年影响因子：5.127 ）

ISSN： 1999-4915

年卷期： 2019 年 11 卷 7 期

页码：

收录情况： SCI

摘要： Peste des petits ruminants virus (PPRV) is associated with global peste des petits ruminants resulting in severe economic loss. Peste des petits ruminants virus dampens host interferon-based signaling pathways through multiple mechanisms. Previous studies deciphered the role of V and C in abrogating IFN-beta production. Moreover, V protein directly interacted with signal transducers and activators of transcription 1 (STAT1) and STAT2 resulting in the impairment of host IFN responses. In our present study, PPRV infection inhibited both IFN-beta- and IFN-gamma-induced activation of IFN-stimulated response element (ISRE) and IFN-gamma-activated site (GAS) element, respectively. Both N and P proteins, functioning as novel IFN response antagonists, markedly suppressed IFN-beta-induced ISRE and IFN-gamma-induced GAS promoter activation to impair downstream upregulation of various interferon-stimulated genes (ISGs) and prevent STAT1 nuclear translocation. Specifically, P protein interacted with STAT1 and subsequently inhibited STAT1 phosphorylation, whereas N protein neither interacted with STAT1 nor inhibited STAT1 phosphorylation as well as dimerization, suggesting that the N and P protein antagonistic effects were different. Though they differed in their relationship to STAT1, both proteins blocked JAK-STAT signaling, severely negating the host antiviral immune response. Our study revealed a new mechanism employed by PPRV to evade host innate immune response, providing a platform to study the interaction of paramyxoviruses and host response.

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