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2009H1N1流感病毒对A549细胞和BEAS-2B细胞作用的初步研究

Preliminary study on cellular effect of A549 and BEAS-2B cells infected by 2009H1N1 influenza virus
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摘要 目的探求2009H1N1流感病毒对A549细胞和BEAS-2B细胞作用,为研究2009H1N1流感病毒的致病机理提供线索。方法不同来源(死亡、重症、普通病例分离)的2009H1N1流感病毒和季节性H1N1流感病毒分别感染A549和BEAS-2B细胞12、24、48、72h后用流式细胞术检测细胞凋亡和细胞周期。结果感染A549细胞12和24h,普通病例分离的2009H1N1流感病毒组的细胞凋亡率最高(P<0.05),重症组的细胞凋亡率最低(P<0.05);48h和72h,死亡组细胞凋亡率最高(P<0.05)。感染BEAS-2B细胞12h,重症组细胞凋亡率最高(P<0.05);48h,死亡组和重症组细胞凋亡率高(P<0.05);72h,死亡组和普通组细胞凋亡率高(P<0.05)。4株病毒主要将A549细胞阻滞在S期,将BEAS-2B细胞阻滞在G0/G1期。结论在细胞凋亡和细胞周期的细胞学观察水平上2009H1N1流感病毒和季节性H1N1流感病毒之间存在差异,不同来源的2009H1N1流感病毒之间也存在差异。 In the study, we aim to detect the effect of A549 and BEAS-2B cells infected by 2009H1N1 influenza virus and to provide clues for the study of pathogenicity mechanism of 2009H1N1 influenza virus. A549 and BEAS 2B cells were in- fected by 2009H1N1 influenza viruses (isolated from death cases, severe cases, and ordinary cases) and the seasonal H1NI in fluenza virus, respectively. Cells were monitored by flow cytomery to detect cell apoptosis and cell cycle after 12, 24, 48 and 72 hours post-infection with viruses. The highset apoptotlc percentage of A549 cells in 12 and 24 hours post infection was in viru ses isolated from ordinary case (P〈0.05), simultaneously. The viruses isolated from severe case was the lowest (P%0.05), and that isolated from death cases was the hightest after 48 and 72 hours post infection (P%0.05). The highest apoptotic per- centage of BEAS-2B cells in 12 hours post-infection was viruses isolated from ordinary case (P〈0.05) ; that of viruses isolated from death and severe cases were higher after 48 hours post-infection (P%0.05); the viruses isolated from death and ordinary cases were high in 72 hours post infection (P〈0.05). Results suggest that the A549 cells are inhibited in Sphase post infec- tion, however, BEAS-2B cells are inhibited in G0/G1 phase. There are differences between 2009H1N1 influenza virus and sea- sonal H1N1 influenza virus in the cytological level of cell apoptosis and ceil cycle, simultaneously, and there are differences a- mong 2009H1N1 influenza viruses.
出处 《中国人兽共患病学报》 CAS CSCD 北大核心 2013年第11期1080-1083,共4页 Chinese Journal of Zoonoses
基金 深圳市科技计划重点项目(2010011)~~
关键词 2009H1N1流感病毒 A549和BEAS-2B细胞 细胞凋亡 细胞周期 2009HIN1 influenza virus A549 and BEAS-2B cells cell apoptosis cell cycle
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参考文献18

  • 1Smith GJ, Vijaykrishna D, Bahl J, et al. Origins and evolution- ary genomics of the 2009 swine-origin H1N1 influenza A epidem- ic[J]. Nature, 2009, 459(7250): 1122 1125. DOI: 10. 1038/ nature08182.
  • 2Chang LY, Shih SR, Shao PL, et al. Novel swine-origin influen-za virus A(HIN1): the first pandemic of the 21t century[J]. J Formos Med Assoc, 2009, 108(7): 526-532. DOI: 10. 1016/ S0929 6646(09)60369-7.
  • 3Garten RJ, Davis CT, Russell CA, et al. Antigenic and genetic characteristics of swine-origin 2009 A (H1N1) influenza viruses circulating in humans[J]. Science, 2009, 325(5937): 197-201. DOh 10. l126/science. 1176225.
  • 4de Jong MD, Simmons CP, Thanh TT, et al. Fatal outcomes of human influenza A(HSN1) is associated with high viral load and hyper cytokinemia[J]. Nat Med, 2006, 12(10): 1203-1207. DOI.. 10. 1038/nm1477.
  • 5Daidoji T, Koma T, Du A, et al. H5N1 avian influenza virus in- duces apoptotic cell death in mammalian airway epithelial cells [J]. J Virol, 2008, 82(22): 11294-11307. DOI: 10.1128/JVI. 01192-08.
  • 6Kandun IN, Wibisono H, Sedyaningsih ER, et al. Three Indo- nesian clusters of HSN1 virus infeetion in 2005[J]. N Engl J Med, 2006, 355(21): 2186-2194.
  • 7Oner AF, Bay A, Arsian S, et al. Avian influenza A(H5N1) in- fection in eastern Turkey in 2006[J]. N Engl J Med, 2006,355 (21): 2179-2185. DOI: 10.1056/NEJMoa060930.
  • 8Chan MC, Cheung CY, Chui WH, et al. Proinflammatory cyto- kine responses induced by influenza A (H5N1) viruses in primary human alveolar and bronchial epithelial cells[J]. Respir Res, 2005, 6.. 135.
  • 9Guan Y, Poon LL, Cheung CY, et al. H5N1 influenza: a prote- an pandemic threat[J]. Proe Natl Aead Sei U S A, 2004, 101 (21) .- 8156-8161. DOI: 10. 1073/pnas. 0402443101.
  • 10Conenello GM, Zamarin D, Perrone LA, et al. A single muta- tion in the PB1-F2 of HSN1 (HK/97) and 1918 influenza A vi- ruses contributes to increased virulence [J]. PLoS Pathog, 2007, 3(10) 1414-1421. DOI.. 10. 1371/journal. ppat. 0030141.

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