Abstract
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.
Highlights
Since March 2013, A novel H7N9 influenza virus first crossed the species barrier and infected humans in East China, causing disease with unusually high morbidity and mortality
A total of 11,12,33 protein spots were found to be differentially expressed in A549 cells infected with H7N9 and H1N1pdm09 influenza virus at 24, 48, 72hpi, respectively (Tables 1, 2 and 3), 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)
The results further prove that the H7N9 virus seriously affect the synthesis of PAFAH1B2 in A549 cells in the later phase of infection
Summary
Since March 2013, A novel H7N9 influenza virus first crossed the species barrier and infected humans in East China, causing disease with unusually high morbidity and mortality. It is a reassortant virus which consists of the gene fragments from earlier H7N9, H7N3 and H9N2 viruses [1,2,3]. Unlike the H1N1pdm, the H7N9 influenza virus has never been extensively circulated among the humans, so the lacking of preexisting immunity presents the human population at high risk [10,11]. A549 cells are widely used for the investigation of influenza A virus replication in vitro or in other proteome studies. The fluorescent two dimensional difference gel electrophoresis (2D-DIGE) and MALDI-TOF–MS/MS were applied to investigate the difference in host proteome after infection with the two influenza virus strains and explored the underlying pathogenic mechanism of H7N9 infection in mammals
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