Preliminary Proteomic Analysis of A549 Cells Infected with Avian Influenza Virus H7N9 and Influenza A Virus H1N1.
Preliminary Proteomic Analysis of A549 Cells Infected with Avian Influenza Virus H7N9 and Influenza A Virus H1N1.
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DOI：
10.1371/journal.pone.0156017
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Fang S
中科院分区：
文献类型：
--
作者：
Ding X;Lu J;Yu R;Wang X;Wang T;Dong F;Peng B;Wu W;Liu H;Geng Y;Zhang R;Ma H;Cheng J;Yu M;Fang S
一种新出现的H7N9流感病毒对人类构成高风险。然而，该病毒的致病机制仍不清楚。应用蛋白质组学方法（2D-DIGE结合MALDI-TOF-MS/MS）研究H7N9流感病毒和H1N1甲型流感病毒（H1N1，pdm 09）感染后24、48和72 h（hpi）原代人肺泡腺癌上皮细胞（A549）的时间反应。有11、12和33个蛋白质表达差异显著在24、48、72 hpi时，尤其是F-肌动蛋白帽蛋白亚单位α 1（CAPZA 1）、鸟氨酸氨基转移酶（OAT）、多聚腺苷酸结合蛋白1（PCBP 1）、蛋白质印迹分析证实了真核翻译起始因子5A-1（EIF 5A）和血小板活化因子乙酰水解酶ⅠB β亚基（PAFAH 1B 2）的存在。功能分析表明，A549细胞中的差异蛋白参与调节细胞病变效应。其中，CAPZA 1、OAT、PCBP 1、EIF 5A的下调与H7N9流感病毒感染细胞的死亡有关。这是首次表明PAFAH 1B 2的下调与H7N9流感病毒感染患者的后期临床症状有关。这些发现有助于从蛋白质组学角度深入了解H7N9流感病毒的致病机制。
A newly emerged H7N9 influenza virus poses high risk to human beings. However, the pathogenic mechanism of the virus remains unclear. The temporal response of primary human alveolar adenocarcinoma epithelial cells (A549) infected with H7N9 influenza virus and H1N1 influenza A virus (H1N1, pdm09) were evaluated using the proteomics approaches (2D-DIGE combined with MALDI-TOF-MS/MS) at 24, 48 and 72 hours post of the infection (hpi). There were 11, 12 and 33 proteins with significant different expressions (P<0.05) at 24, 48 and 72hpi, especially F-actin-capping protein subunit alpha-1 (CAPZA1), Ornithine aminotransferase (OAT), Poly(rC)-binding protein 1 (PCBP1), Eukaryotic translation initiation factor 5A-1 (EIF5A) and Platelet-activating factor acetylhydrolaseⅠb subunit beta (PAFAH1B2) were validated by western-blot analysis. The functional analysis revealed that the differential proteins in A549 cells involved in regulating cytopathic effect. Among them, the down-regulation of CAPZA1, OAT, PCBP1, EIF5A are related to the death of cells infected by H7N9 influenza virus. This is the first time show that the down-regulation of PAFAH1B2 is related to the later clinical symptoms of patients infected by H7N9 influenza virus. These findings may improve our understanding of pathogenic mechanism of H7N9 influenza virus in proteomics.