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目的分析江苏省2012-2013年流行的柯萨奇病毒A组6型(coxsackievirus A6,CV-A6)毒株VP1区序列特征。方法采集江苏省2012-2013年10例CV-A6感染引发的手足口病(hand,foot and mouth disease,HFMD)患儿的咽拭子或肛拭子样本,通过RT-PCR扩增完整VP1区。应用DNAStar软件包的MegAlign对CV-A6毒株的VP1区进行核苷酸和氨基酸序列比对分析,构建系统进化树。结果同源性和系统进化分析结果显示,10株流行株与2008年芬兰流行株同属于分支F,核苷酸同源性为95.1%~96.5%,而与原型株Gdula核苷酸同源性较低,为82.4%~84.0%。01-PZ/JS/2012、02-PZ/JS/2012、03-PZ/JS/2012、04-BY/JS/2012和08-PZ/JS/2013属于分支F2,05-PZ/JS/2013、06-PZ/JS/2013、07-PZ/JS/2013、09-PZ/JS/2013和10-BY/JS/2013属于F3,不同亚分支毒株之间核苷酸同源性为95.8%~97.2%。结论江苏省2012-2103年流行的10株毒株分别属于F2和F3分支,属于F2的5株毒株的VP1第30位氨基酸位点为V,而属于F3的5株毒株该位点为A。开展CV-A6流行株分子流行病学研究,了解毒株进化变异的趋势,对防控CV-A6引发的HFMD具有重要意义。
Objective To analyze the sequence characteristics of the VP1 region of coxsackievirus A6 (CV-A6) strain that is prevalent in Jiangsu province during 2012-2013. Methods Throat swabs or anal swab samples of 10 children with hand, foot and mouth disease (HFMD) induced by CV-A6 infection in Jiangsu province from 2012 to 2013 were collected. The complete VP1 region was amplified by RT-PCR . The nucleotide and amino acid sequence alignment of the VP1 region of the CV-A6 strain was performed using the DNAStar software package MegAlign to construct the phylogenetic tree. Results The results of homology and phylogenetic analysis showed that the 10 strains belong to the same branch F as the 2008 Finnish strains, and their nucleotide homology was 95.1% ~ 96.5% Low, 82.4% ~ 84.0%. 01-PZ / JS / 2012, 02-PZ / JS / 2012, 03-PZ / JS / 2012, 04-BY / JS / 2012 and 08-PZ / JS / 2013 belong to branch F2,05-PZ / JS / 2013 F3, the nucleotide homology between different sub-strain strains was 95.8 % ~ 97.2%. CONCLUSION: The 10 strains of strains that were endemic to Jiangsu province between 2012 and 2103 belonged to the F2 and F3 branches, respectively. The 5 strains belonging to F2 had VP1 at amino acid 30 and the 5 strains belonging to F3 were A. To carry out molecular epidemiological studies of CV-A6 epidemic strains to understand the trend of evolutionary variation of the strains is of great significance for preventing and controlling HFMD induced by CV-A6.