Dataset for: iTRAQ-based proteomic and bioinformatic characterization of human mast cell upon different IAV (H1N1 and H5N1) infection

In our previous study, it was demonstrated that mast cell can support replication of Influenza A virus (IAV) and how this occurs is poorly understood. At present, using quantitative mass spectrometry, we analyzed proteome of human mast cells (HMCs) infected with different IAV strains at 12h post-infection (12 hpi). More 41 differentially expressed proteins (DEPs) of global HMCs caused by H5N1 (A/Chicken/Henan/1/04) virus than H1N1 (A/WSN/33) virus. Bioinformatic analyses confirmed that H1N1 significantly regulated the RNA degradation pathway via CNOT4 expressing highly while apoptosis could be suppressed by H5N1 virus down regulated by p53 signaling pathway with P≤0.05 at 12 hpi. HIF-1 signal pathway of HMCs was more susceptible to the infection of H5N1 than H1N1 virus.

本团队前期研究已证实，肥大细胞可支持甲型流感病毒（Influenza A virus, IAV）的增殖，但其具体调控机制尚未阐明。本研究采用定量质谱（quantitative mass spectrometry）技术，对感染不同IAV毒株后12小时（12 hpi）的人类肥大细胞（human mast cells, HMCs）开展全局蛋白质组学分析。结果显示，相较于H1N1（A/WSN/33）病毒，H5N1（A/Chicken/Henan/1/04）病毒感染诱导的HMCs差异表达蛋白（differentially expressed proteins, DEPs）数量多出41种。生物信息学分析结果证实，在感染后12小时，H1N1病毒可通过高表达CNOT4显著调控RNA降解通路；而H5N1病毒则可通过下调p53信号通路抑制细胞凋亡，上述两项调控均具有P≤0.05的统计学显著性。相较于H1N1病毒，HMCs的缺氧诱导因子-1（hypoxia-inducible factor-1, HIF-1）信号通路对H5N1病毒感染更为易感。