Global quantitative proteomic analysis profiles host protein expression in response to Sendai virus infection
Global quantitative proteomic analysis profiles host protein expression in response to Sendai virus infection
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全球定量蛋白质组分析描绘了仙台病毒感染后宿主蛋白的表达
DOI：
10.1002/pmic.201600239
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发表时间：
2017
期刊：
影响因子：
3.4
通讯作者：
Zhang Lei-Ke
中科院分区：
文献类型：
--
作者：
Zhu Sheng-Lin;Chen Xi;Wang Liang-Jie;Wan Wei-Wei;Xin Qi-Lin;Wang Wei;Xiao Gengfu;Zhang Lei-Ke
仙台病毒(Sendai Virus，SeV)是一种囊膜非节段性负链RNA病毒，属于副粘病毒科响应性病毒属。作为一种模式病原体，SEV已被广泛研究以确定副粘病毒的基本生化和分子生物学特性。此外，SeV感染的宿主细胞被广泛用于揭示先天免疫反应的机制。为了确定SeV感染过程或SeV诱导的先天性免疫反应过程中涉及的蛋白质，已经对SeV与宿主的相互作用进行了系统范围的评估。基因芯片、siRNA筛选和磷酸化蛋白质组学分析表明，SeV感染过程中涉及多条信号通路。在这里，为了研究SeV与宿主的相互作用，对SeV感染的HEK 293T细胞进行了全局定量蛋白质组学分析。共有4699个宿主蛋白被量化，其中742个蛋白是差异调控的。生物信息学分析表明，调节蛋白主要参与“干扰素-I信号通路”和“对病毒的防御反应”，提示这些过程在SeV感染中起作用。进一步的基于RNAi的功能研究表明，调节蛋白三方基序(TRIM24)和TRIM27影响SeV诱导的干扰素-I的产生。我们的数据提供了宿主细胞对SeV的反应的综合视图，并确定了参与SeV感染过程或SeV诱导的天然免疫反应过程的宿主蛋白。
Sendai virus (SeV) is an enveloped nonsegmented negative‐strand RNA virus that belongs to the genusRespirovirusof theParamyxoviridaefamily. As a model pathogen, SeV has been extensively studied to define the basic biochemical and molecular biologic properties of the paramyxoviruses. In addition, SeV‐infected host cells were widely employed to uncover the mechanism of innate immune response. To identify proteins involved in the SeV infection process or the SeV‐induced innate immune response process, system‐wide evaluations of SeV–host interactions have been performed. cDNA microarray, siRNA screening and phosphoproteomic analysis suggested that multiple signaling pathways are involved in SeV infection process. Here, to study SeV–host interaction, a global quantitative proteomic analysis was performed on SeV‐infected HEK 293T cells. A total of 4699 host proteins were quantified, with 742 proteins being differentially regulated. Bioinformatics analysis indicated that regulated proteins were mainly involved in “interferon type I (IFN‐I) signaling pathway” and “defense response to virus,” suggesting that these processes play roles in SeV infection. Further RNAi‐based functional studies indicated that the regulated proteins, tripartite motif (TRIM24) and TRIM27, affect SeV‐induced IFN‐I production. Our data provided a comprehensive view of host cell response to SeV and identified host proteins involved in the SeV infection process or the SeV‐induced innate immune response process.