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| 新型甲型H7N9流感病毒血凝素基因进化分析 |
| 关蔚,李自雄,林吉,韩一芳,苏彤,殷建华,张宏伟,曹广文* |
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(第二军医大学热带医学与公共卫生学系流行病学教研室,上海市医学生物防护重点实验室,上海 200433
*通信作者) |
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| 摘要: |
| 目的 探讨2013年4月流行的新型甲型H7N9禽流感病毒的表面蛋白血凝素(HA)基因的进化，以及氨基酸的变异情况。方法 从美国国家生物技术信息中心(NCBI)和全球禽流感基因共享数据库(GISAID)中下载H7N9流感病毒以及有代表性的H7N2、H7N3、H7N7亚型流感病毒的HA基因序列,运用Molecular Evolutionary Genetics Analysis (MEGA) version 5.05软件进行序列分析,用邻接法构建基因进化树；通过氨基酸序列分析HA蛋白受体结合位点、糖基化位点和裂解位点的变化。结果 2013年新型甲型H7N9流感病毒与2011年浙江禽类H7N3流感病毒株(JQ906573.1)的相似性达到95.3%～95.6%；受体结合位点氨基酸发生变异,为Q226L,5个糖基化位点高度保守；HA裂解位点位于aa339和aa340之间,仅有1个碱性氨基酸:R。结论 2013年新型甲型H7N9流感病毒HA基因是由中国禽类H7亚型进化而来,Q226L变异导致的受体结合位点的变化可能是新型流感病毒具有人感染性的原因。 |
| 关键词: H7N9亚型流感病毒A型 血凝素类 进化 变异(遗传学) |
| DOI：10.3724/SP.J.1008.2013.00595 |
| 投稿时间：2013-05-09修订日期：2013-05-22 |
| 基金项目:上海市公共卫生重点学科建设项目(12GWZX0102). |
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| Phylogenetic analysis of hemagglutinin (HA) gene of the novel avian influenza virus A/H7N9 |
| GUAN Wei,LI Zi-xiong,LIN Ji,HAN Yi-fang,SU Tong,YIN Jian-hua,ZHANG Hong-wei,CAO Guang-wen* |
(Department of Epidemiology, Faculty of Tropical Medicine and Public Health, Second Military Medical University, Shanghai Key Laboratory of Medical Biodefense, Shanghai 200433, China
*Corresponding author.) |
| Abstract: |
| Objective To investigate the evolution and variations in coding amino acids of hemagglutinin (HA) gene of the novel avian influenza virus H7N9 in 2013 epidemic. Methods The HA gene sequences of influenza virus H7N9, H7N2, H7N3 and H7N7 subtypes were downloaded from the database of The National Center for Biotechnology Information (NCBI) and The Global Initiative on Sharing All Influenza Data (GISAID). MEGA 5.05 software was used for sequence analysis and N-J method was used for constructing the phylogenetic trees. The amino acid sequences at the receptor binding sites, glycosylation sites, and cleavage sites was aligned and analyzed. Results The HA genes this novel A/H7N9 virus in 2013 shared a 95.3%-95.6% similarity with JQ906573.1|Zhejiang (H7N3 virus) isolated in 2011. The most important variation in this novel H7N9 isolates was found at the receptor binding site: Q226L. The 5 glycosylation sites were highly conservative. One basic amino acid (R) at the HA cleavage sites, located between aa339 and aa340, was also found in this novel isolate. Conclusion The HA gene of this novel H7N9 isolate might originate from H7 subtypes carried by birds in China. The binding site change caused by Q226L variation might be responsible for human infection of this novel H7N9 isolate. |
| Key words: H7N9 subtype influenza A virus hemagglutinins evolution variation (genetics) |
