2010年南京人群甲型H3N2流感分离毒株全基因组特性分析

来源 :中国人兽共患病学报 | 被引量 : 0次 | 上传用户:sinbala
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目的分析2010年南京地区甲型H3N2流感病毒的分子特征和演化趋势。方法测定2010年期间所分离3株病毒的8个RNA片段的核苷酸序列。构建各个基因基于核苷酸序列的系统发生树,并分析分离毒株与参考毒株11个基因特定氨基酸位点的变异情况。结果在3株病毒中,未发生片段间的重配。以A/Perth/16/2009为参考,3个分离毒株发生在HA和NA蛋白抗原决定簇的氨基酸变异均数分别为5.7和1.3;以A/Brisbane/10/2007为参考,3株病毒PB1的第375位发生突变(S→G),Nanjing/1655和Nanjing/1663的PB1-F2蛋白第26位缺失。另外3株病毒M2的金刚烷胺耐药位点(31位)为N。结论所测3株流感病毒HA基因的氨基酸变异可能导致新流行株的形成,病毒对金刚烷胺耐受而对神经氨酸酶抑制剂敏感。病毒的PB1第375位和PB1-F2第26位的变异可能成为H3N2病毒新的进化方向。 Objective To analyze the molecular characteristics and evolution trend of influenza A (H3N2) virus in Nanjing in 2010. Methods The nucleotide sequences of eight RNA fragments of three viruses isolated during 2010 were determined. The phylogenetic tree based on nucleotide sequence of each gene was constructed and the variation of specific amino acid sites of 11 genes of isolated strains and reference strains was analyzed. Results Among the three viruses, no recombination occurred between the fragments. Taking A / Perth / 16/2009 as reference, the mean number of amino acid variation of the three isolates was between 5.7 and 1.3 for HA and NA antigenic determinants, respectively. A / Brisbane / 10/2007 was used as reference and three isolates The mutation at position 375 of PB1 (S → G) and deletion of the PB1-F2 protein at Nanjing / 1655 and Nanjing / 1663 at position 26 were observed. The amantadine resistance site (position 31) of the other three viruses M2 was N. Conclusion The amino acid variation of the HA genes of the three influenza viruses may lead to the formation of a new epidemic strain. The virus is resistant to amantadine and sensitive to neuraminidase inhibitors. The mutation of the 375th PB1 and the 26th PB1-F2 of the virus may be the new evolutionary direction of H3N2 virus.
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