The 2009 pandemic A/Wenshan/01/2009 H1N1 induces apoptotic cell death in human airway epithelial cells
作者机构:State Key Laboratory of Medical Molecular BiologyInstitute of Basic Medical SciencesPeking Union Medical CollegeTsinghua UniversityChinese Academy of Medical SciencesBeijing 100005China Department of Viral ImmunologyInstitute of Medical BiologyChinese Academy of Medicine SciencePeking Union Medical CollegeKunming 650118China State Key Laboratory of Pathogen and BiosecurityBeijing Institute of Microbiology and EpidemiologyBeijing 100071China Centre for Disease Prevention and ControlCheng Du Military RegionKunming 650032China Shanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai 200031China
出 版 物:《Journal of Molecular Cell Biology》 (分子细胞生物学报(英文版))
年 卷 期:2011年第3卷第4期
页 面:221-229页
核心收录:
学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金:supported by the Ministry of Science and Technology(2009CB522105) the Ministry of Health(2009ZX10004-308)of China support of the Science and Technology Commission of Shanghai Municipality(07pj14096)
主 题:apoptosis respiratory S-OIV H1N1 influenza virus
摘 要:In 2009,a novel swine-origin H1N1 influenza virus emerged in Mexico and quickly spread to other countries,including *** 2009 pandemic H1N1 can cause human respiratory disease,but its pathogenesis remains poorly ***,we studied the infection and pathogenesis of a new 2009 pandemic strain,A/Wenshan/01/2009 H1N1,in China in human airway epithelial cell lines compared with contemporary seasonal H1N1 influenza *** results showed that viral infection by the A/Wenshan H1N1 induced significant apoptotic cell death in both the human nasopharyngeal carcinoma cell line CNE-2Z and the human lung adenocarcinoma cell line *** A/Wenshan H1N1 virus enters both of these cell types more efficiently than the seasonal influenza *** entry in both cell lines was shown to be mediated by clathrin-and dynamin-dependent ***,we discovered that the 2009 pandemic H1N1 strain,A/Wenshan/01/2009,can induce apoptotic cell death in epithelial cells of the human respiratory tract,suggesting a molecular pathogenesis for the 2009 pandemic H1N1.