2009年新型甲型H1N1流感病毒聚合酶编码基因的遗传特性及重要功能位点变异分析

Genetic characteristics and variations at important functional sites of polymerase coding genes of the novel A/H1N1 influenza pandemic virus in 2009

目的分析2009年新型甲型H1N1流感病毒聚合酶PA、PB1和PB2编码基因序列遗传的进化特征及重要功能位点变异。方法从NCBI流感数据库中获取此次流行株的PA、PB1和PB2聚合酶编码基因序列以及不同年代、不同地区、不同宿主、不同亚型的参考序列,运用MEGA 4.0软件比对和修剪此次流行株的代表序列和所有参考株序列。并用NJ法构建进化树,同时比对此次流行株的代表序列、各年代人的A/H1N1以及禽流感病毒参考序列等编码的PB2蛋白质序列。结果不同地区、不同时间分离的2009年新型甲型H1N1流感病毒的聚合酶PA、PB1和PB2编码基因同源性均>99.8%,且聚集在一枝独特的进化枝上,与禽流感病毒接近。进化树显示三者来源皆为禽类,目前仍未发生突变;PB2的重要功能位点第627位氨基酸为谷氨酸,具有禽流感病毒的特点。结论本次流感大流行为新型甲型H1N1病毒导致的同源爆发,但还不具备典型的高致病性,禽流感病毒可能参与了聚合酶基因的重排过程。

[ Objective To elucidate the hereditary characteristics and variations of important functional domains of polymerase PA, PB1 and PB2 gene of the novel A/HIN1 influenza pandemic virus in 2009. Methods The sequences of PA, PB1 and PB2 gene of the novel A/HIN1 strains, and the reference sequences according to the years, locations, hosts and subtypes of influenza virus were retrieved from NCBI database. All the sequences were contrasted with MEGA4. 0 software. The phylogenetic tree was constructed with the neighborjoining method. All the deduced PB2 protein sequences were compared among the influenza strains, the avian influenza virus and the human A/H1N1 influenza virus found in different years. Results The sequence homology exceeded 99. 8% of PA, PB1 and PB2 gene of the novel A/HIN1 influenza virus isolated from different locations and different time. The sequences of PA, PB1 and PB2 gene isolated from different locations and time showed a high homology, clustered in a unique new clade, and close to avain influenza virus. Phylogenesis indicated that all the PA, PB1 and PB2 gene originally evolved from avain influenza virus. Alignments of the deduced protein sequences showed that the 627th amino acid of the PB2 gene of novel A/H1N1 strains was glutamic acid （Glu）, which was the same as that of avian influenza virus, rather than human HIN1 virus. Conclusions The novel A/H1N1 influenza virus from the same origin leads to the outbreak in 2009, and it is of atypical high pathogenicity. The polyrnerase gene of avian influenza virus might partially reassort with the novel A/H1N1 virus.