Primary study on the lesions and specific proteins in BEAS-2B cells induced with the 2009 A (H1N1) influenza virus

• DOI: 10.1007/s00253-014-5852-y
• Publication Date: 2014-06-05T03:56:22Z
• Authors: Shisong Fang; Kaining Zhang; Ting Wang; Xin Wang; Xing Lu; Bo Peng; Weihua Wu; Ran Zhang; Shiju Chen; Renli Zhang; Hong Xue; Muhua Yu; Jinquan Cheng
• Keywords: 0301 basic medicine; Time Factors; 2009 H1N1 influenza virus; Proteome; Cell Cycle; Proteins; Apoptosis; Epithelial Cells; Flow Cytometry; Mass Spectrometry; Cell Line; 3. Good health; Two-dimensional electrophoresis; 03 medical and health sciences; Influenza A Virus, H1N1 Subtype; BEAS-2B cells; Host-Pathogen Interactions; Influenza, Human; Humans; Differential proteins; Electrophoresis, Gel, Two-Dimensional

In order to investigate the lesions and proteins with differential expression in cells infected with the 2009 A (H1N1) virus and to determine the specific proteins involved in cell damage, the present study has been performed. BEAS-2B cells were infected with the 2009 A (H1N1) influenza virus or the seasonal H1N1 influenza virus for 12, 24, 48, and 72 h, and cell cycle and apoptosis were analyzed with flow cytometry. Total cellular proteins were extracted and underwent two-dimensional gel electrophoresis. The differentially expressed proteins underwent mass spectrometry for identification. The results showed that after 12 h, cells infected with the virus strain sourced from severe cases had the highest apoptosis rate (P < 0.05). After 48 h, cells infected with the virus strain sourced from fatal cases and severe cases had the highest apoptosis rate (P < 0.05), and after 72 h, cells infected with virus strains from fatal cases and ordinary cases had the highest apoptosis rate (P < 0.05). All the four influenza virus strains induced cell cycle arrest mainly at the G0/G1 phase. Eighteen differentially expressed proteins were identified, including galectin-1, cofilin-1, protein DJ-1, proteasome subunit α type-5, macrophage migration inhibitory factor, translationally controlled tumor protein, profilin 1, and interferon α-2. Galectin-1 was specifically observed in BEAS-2B infected with 2009 A (H1N1) influenza viruses, and cofilin-1 was specifically observed in BEAS-2B cells in the late stage of 2009 A (H1N1) influenza virus infection. In conclusion, differential effects of the 2009 A (H1N1) influenza virus and seasonal H1N1 influenza virus were identified on the cell cycle and apoptosis, and galectin-1 may play a role in cell apoptosis induced by 2009 A (H1N1) influenza virus.