To explore the mechanisms of influenza H7N9 virus pathogenesis, influenza H7N9 virus and H1N1 influenza A virus(H1N1pdm09)-infected A549 cellular models were established, and differential protein expression in A549 cells infected with the two strains were investigated.A549 cells were infected with H7N9 and H1N1pdm09influenza virus at a multiplicity of infection(MOI)of 0.001.The temporal response of A549 cells infected with the two strains was evaluated using the proteomics approaches(2DDIGE combined with MALDI-TOF-MS/MS)at 24,48 and 72hours post infection(hpi).There were 11,12 and 33proteins with significantly different expression at 24,48 and 72hpi,respectively.Compared with H1N1pdm09 infection, functional analysis revealed that the down-regulation of proteins in H7N9 infection including F-actin-capping protein subunit alpha-1(CapZ-α1), ornithine aminotransferase(OAT),poly(rC)-binding protein 1(PCBP1)and eukaryotic translation initiation factor 5A-1(eIF5A)produced cytopathic effects. The down-regulation of platelet-activating factor acetylhydrolaseIb subunit beta(PAFAH1B2)in H7N9-infection may be related to the clinical symptoms of patients infected by the influenza H7N9 virus.
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