Zhu Sheng-Lin, Chen Xi, Wang Liang-Jie, Wan Wei-Wei, Xin Qi-Lin, Wang Wei, Xiao Gengfu, Zhang Lei-Ke
State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, P. R. China.
The Laboratory of Biological Mass Spectrometry, Wuhan Institute of Biotechnology, Wuhan, P. R. China.
Proteomics. 2017 Mar;17(5). doi: 10.1002/pmic.201600239.
Sendai virus (SeV) is an enveloped nonsegmented negative-strand RNA virus that belongs to the genus Respirovirus of the Paramyxoviridae family. 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.
仙台病毒（SeV）是一种有包膜的非节段性负链RNA病毒，属于副粘病毒科呼吸病毒属。作为一种模式病原体，人们对仙台病毒进行了广泛研究，以确定副粘病毒的基本生化和分子生物学特性。此外，感染仙台病毒的宿主细胞被广泛用于揭示先天免疫反应的机制。为了鉴定参与仙台病毒感染过程或仙台病毒诱导的先天免疫反应过程的蛋白质，人们对仙台病毒与宿主的相互作用进行了全系统评估。cDNA微阵列、siRNA筛选和磷酸化蛋白质组分析表明，多个信号通路参与了仙台病毒感染过程。在此，为了研究仙台病毒与宿主的相互作用，对感染仙台病毒的人胚肾293T细胞进行了全基因组定量蛋白质组分析。总共对4699种宿主蛋白进行了定量分析，其中742种蛋白受到差异调节。生物信息学分析表明，受调节的蛋白主要参与“Ⅰ型干扰素（IFN-Ⅰ）信号通路”和“对病毒的防御反应”，这表明这些过程在仙台病毒感染中发挥作用。进一步基于RNA干扰的功能研究表明，受调节的蛋白，即三联基序（TRIM24）和TRIM27，影响仙台病毒诱导的IFN-Ⅰ产生。我们的数据提供了宿主细胞对仙台病毒反应的全面视图，并鉴定了参与仙台病毒感染过程或仙台病毒诱导的先天免疫反应过程的宿主蛋白。
