论文部分内容阅读
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。
Objective To investigate the evolution of the surface hemagglutinin (HA) gene of new type A H7N9 avian influenza virus and its amino acid variation in April 2013. Methods The HA gene sequences of H7N9 influenza virus and representative H7N2, H7N3 and H7N7 subtypes were downloaded from the NCBI and GISAID. The sequences were analyzed by Molecular Evolutionary Genetics Analysis (MEGA) version 5.05 software was used to construct the phylogenetic tree. The amino acid sequence was used to analyze the binding site, glycosylation site and cleavage site of HA protein receptor. Results The similarity between the new H7N9 influenza A virus and the Zhejiang avian H7N3 influenza virus strain (JQ906573.1) in 2013 was 95.3% -95.6%. The variation of amino acid at the binding site of the receptor was Q226L and five glycosylation The site is highly conserved; the HA cleavage site is located between aa339 and aa340 with only 1 basic amino acid: R. Conclusion The HA gene of the novel H7N9 influenza A virus was evolved from the H7 subtype of Chinese birds in 2013. The change of receptor binding site induced by the Q226L mutation may be the reason of the human infectious nature of the new influenza virus.