Zhu Ru-nan, Qian Yuan, Wang Fang, Deng Jie, Zhao Lin-qing, Liu Cheng-gui
Laboratory of Virology, Beijing Municipal Laboratory of Infection and Immunity, Capital Institute of Pediatrics, Beijing 100020, China.
Zhonghua Liu Xing Bing Xue Za Zhi. 2006 Mar;27(3):241-4.
To characterize the HA1 regions of hemagglutinin gene of influenza viruses (H3N2) isolated from children in Beijing from 1998 - 2004.
The HA1 regions of hemagglutinin gene were amplified by RT-PCR from the viruses isolated and identified as A3 (H3N2) from clinical samples collected from infants and children during the peak seasons of influenza between 1998 and 2004. PCR products were sequenced or cloned into T-A vector and were analyzed after being sequenced.
The HA1 regions of hemagglutinin genes amplified from those isolates were 987 bp in length, encoding a protein of 329 amino acids in length. The identities of nucleotides and amino acids among these H3N2 isolates in Beijing and vaccines strains from 1998 - 2004 were 95.5% - 100.0% and 93.0% - 100.0%, respectively. The homology of the HA1 regions were related to the date of virus isolation, meaning the homology was higher among those strains isolated in nearer dates than others. Seven potential N-linked glycosylation sites in the HA1 regions located at amino acid positions 8, 22, 38, 63, 126, 165 and 285 were conserved in all the viruses analyzed. Two sites at 122 and 133 were inserted in those virus isolated after 1997, and another site at 144 appeared in those isolated after 1999. More amino acid substitutions located in the five putative antigenic sites or receptor binding sites were found more in the isolates than the isolates from previous year. Phylogenetic analysis showed new branches appeared continuously during 1998 - 2004. The strains isolated during winter in 2004 belonged to different branches, suggesting the appearance of new variants.
Amino acid substitutions continuously occurred in the HA1 regions of hemagglutinin genes in influenza virus (H3N2) isolated from children in Beijing from 1998 - 2004, which might have resulted in antigenic drift and led to the appearance of new variants.
对1998 - 2004年从北京儿童中分离出的流感病毒（H3N2）血凝素基因的HA1区域进行特征分析。
采用RT-PCR方法从1998年至2004年流感流行高峰季节采集的婴幼儿临床样本中分离并鉴定为A3（H3N2）的病毒中扩增血凝素基因的HA1区域。PCR产物进行测序或克隆到T-A载体中，测序后进行分析。
从这些分离株中扩增出的血凝素基因的HA1区域长度为987 bp，编码一个长度为329个氨基酸的蛋白质。北京这些H3N2分离株与1998 - 2004年疫苗株之间核苷酸和氨基酸的同一性分别为95.5% - 100.0%和93.0% - 100.0%。HA1区域的同源性与病毒分离日期有关，即较近日期分离的毒株之间同源性更高。在所有分析的病毒中，HA1区域位于氨基酸位置8、22、38、63、126、165和285的7个潜在N-糖基化位点是保守的。1997年后分离的病毒中在122和133位插入了两个位点，1999年后分离的病毒中在144位出现了另一个位点。在五个假定的抗原位点或受体结合位点中发现的氨基酸替换在分离株中比上一年的分离株更多。系统发育分析表明，1998 - 2004年期间不断出现新的分支。2004年冬季分离的毒株属于不同分支，提示出现了新的变异株。
1998 - 2004年从北京儿童中分离出的流感病毒（H3N2）血凝素基因的HA1区域不断发生氨基酸替换，这可能导致了抗原漂移并导致新变异株的出现。
