Genomic characterization of avian influenza A(H7N9) virus in Zhaoqing, China, 2014-2016
10.3969/j.issn.1002-2694.2017.03.003
- VernacularTitle:2014-2016年广东省肇庆市人感染H7N9禽流感病毒基因组特征分析
- Author:
Hanqing TAN
;
Jieping CHENG
;
Haifang TAN
;
Yingmei ZHU
;
Feng LIN
;
Xiaoqing LIANG
;
Jie CHEN
;
Wei MAI
- Keywords:
human infection with avian influenza A (H7N9) virus;
hemagglutinin gene;
neuraminidase gene;
sequence analysis
- From:
Chinese Journal of Zoonoses
2017;33(3):202-207,240
- CountryChina
- Language:Chinese
-
Abstract:
We analyzed genetic evolution characteristics of avian influenza A (H7N9) virus isolated in Zhaoqing,China,2014-2016.Nucleic acid were extracted and sequenced from 17 samples of H7N9 positive cases in Zhaoqing.Genetic characteristics of homology and important amino acid sites were analyzed by using BioEdit5.0 and MEGA6.0.The evolutionary trees were constructed by Neighbor-Joining and the referenced sequences were downloaded from GenBank,Eight nucleic acid fragments from 7 strains of H7N9 viruses were successfully generated.The highest homology was found in HA gene with A/chicken/Dongguan/695/2014(H7N9),and NA gene with A/chicken/Dongguan/1075/2014(H7N9).The internal genes were high homology with avian H7N9 and H9N2 virus from Dongguan and Shenzhen in Guangdong,China.The HA and NA genes were directly evolved in the Pearl River Delta evolution branch with the H7N9 sequences from the cities of Dongguan,Guangzhou and Shenzhen,while the sequences from the provinces of Anhui,Zhejiang,and Jiangsu were in the Yangtze River Delta evolution branch.There were 2 alkaline amino acids in cleavage site of HA,2 mutations (G186V and Q226L) in the crucial sites related with the receptor of HA protein,1 mutation (E627K) in PB2 protein,and 1 drug resistance mutation (S31N) in M2 protein.And no evidence of neuraminidase resistance in NA protein was found.In conclusion,the H7N9 virus for human infection in Zhaoqing may originate from avian H7N9 and H9N2 viruses,which circulated in the Pearl River Delta region of Guangdong from 2013 to 2014.The mutations of G186V,Q226L and E627 K might be related with high susceptibility to human beings.
