Peste des petits ruminants virus non-structural C protein inhibits the induction of interferon-β by potentially interacting with MAVS and RIG-I.
Peste des petits ruminants virus non-structural C protein inhibits the induction of interferon-β by potentially interacting with MAVS and RIG-I.
复制标题
小反刍兽疫病毒非结构 C 蛋白通过与 MAVS 和 RIG-I 潜在相互作用抑制干扰素-β 的诱导
DOI：
10.1007/s11262-020-01811-y
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发表时间：
2021-03
期刊：
影响因子：
1.6
通讯作者：
Jialin B
中科院分区：
文献类型：
--
作者：
Linjie L;Xiaoling S;Xiaoxia M;Xin C;Ali A;Jialin B
小反刍兽疫病毒（PPRV）主要通过引起天然宿主的免疫抑制而在世界范围内引起家养和野生小反刍动物的急性和高度接触性疾病。有人认为，PPRV的非结构C蛋白有助于逃避宿主反应，但其拮抗宿主反应的分子机制尚未完全表征。在此，我们报告了PPRV C蛋白通过MAVS和RIG-I介导的途径在体外对干扰素-β（IFN-β）表达的拮抗作用。双荧光素酶报告基因分析和IFN-β mRNA直接表达分析表明，PPRV C通过与MAVS和RIG-I信号分子的潜在相互作用显著下调IFN-β。结果进一步表明，PPRV C蛋白在体外显著抑制PPRV、EMCV和SVS感染中内源性和外源性IFN-β诱导的抗病毒作用。此外，PPRV C蛋白不仅下调IFN-β，还下调干扰素刺激基因56（ISG 56）、ISG 15、C-X-C基序趋化因子（CXCL 10）和RIG-I介导的ISRE和NF-κB的IFN启动子元件的激活的下游细胞因子。本研究进一步阐明了PPRV C蛋白可显著抑制STAT 1的磷酸化，干扰JAK-STAT信号通路的信号传递。总的来说，这项研究表明，PPRV C蛋白是重要的先天免疫逃避和疾病的进展。
Peste des petits ruminants virus (PPRV) causes an acute and highly contagious disease in domestic and wild small ruminants throughout the world, mainly by invoking immunosuppression in its natural hosts. It has been suggested that the non-structural C protein of PPRV helps in evading host responses but the molecular mechanisms by which it antagonizes the host responses have not been fully characterized. Here, we report the antagonistic effect of PPRV C protein on the expression of interferon-β (IFN-β) through both MAVS and RIG-I mediated pathways in vitro. Dual luciferase reporter assay and direct expression of IFN-β mRNA analysis indicated that PPRV C significantly down regulates IFN-β via its potential interaction with MAVS and RIG-I signaling molecules. Results further indicated that PPRV C protein significantly suppresses endogenous and exogenous IFN-β-induced anti-viral effects in PPRV, EMCV and SVS infections in vitro. Moreover, PPRV C protein not only down regulates IFN-β but also the downstream cytokines of interferon stimulated genes56 (ISG56),ISG15, C-X-C motif chemokine (CXCL10) and RIG-I mediated activation of IFN promoter elements of ISRE and NF-κB. Further, this study deciphers that PPRV C protein could significantly inhibit the phosphorylation of STAT1 and interferes with the signal transmission in JAK-STAT signaling pathway. Collectively, this study indicates that PPRV C protein is important for innate immune evasion and disease progression.
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