title: Primary study on the lesions and specific proteins in BEAS-2B cells induced with the 2009 A (H1N1) influenza virus.
abstract: 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.
authors.affiliation: Shenzhen Centre for Disease Control and Prevention, No. 8, LongYuan Rd., NanShan District, Shenzhen City, Guangdong Province, People's Republic of China.
authors.forename: Shisong
authors.initials: S
authors.lastname: Fang
authors.forename: Kaining
authors.initials: K
authors.lastname: Zhang
authors.forename: Ting
authors.initials: T
authors.lastname: Wang
authors.forename: Xin
authors.initials: X
authors.lastname: Wang
authors.forename: Xing
authors.initials: X
authors.lastname: Lu
authors.forename: Bo
authors.initials: B
authors.lastname: Peng
authors.forename: Weihua
authors.initials: W
authors.lastname: Wu
authors.forename: Ran
authors.initials: R
authors.lastname: Zhang
authors.forename: Shiju
authors.initials: S
authors.lastname: Chen
authors.forename: Renli
authors.initials: R
authors.lastname: Zhang
authors.forename: Hong
authors.initials: H
authors.lastname: Xue
authors.forename: Muhua
authors.initials: M
authors.lastname: Yu
authors.forename: Jinquan
authors.initials: J
authors.lastname: Cheng
mesh_terms: D017209:Apoptosis; D002453:Cell Cycle; D002460:Cell Line; D015180:Electrophoresis, Gel, Two-Dimensional; D004847:Epithelial Cells / Q000737:chemistry* / Q000821:virology*; D005434:Flow Cytometry; D054884:Host-Pathogen Interactions; D006801:Humans; D053118:Influenza A Virus, H1N1 Subtype / Q000254:growth & development* / Q000302:isolation & purification; D007251:Influenza, Human / Q000821:virology; D013058:Mass Spectrometry; D011506:Proteins / Q000032:analysis*; D020543:Proteome / Q000032:analysis*; D013997:Time Factors
chemical_list: D011506:Proteins; D020543:Proteome