Molecular evolution of influenza A/H3N2 viruses HA and NA genes circulating in Shenzhen in 2017
10.16462/j.cnki.zhjbkz.2019.09.019
- Author:
Ying FAN
1
;
Xue-yun LI
;
Shi-song FANG
;
Bo PENG
Author Information
1. School of public health, Shenzhen Campus, Sun Yat-Sen University, Shenzhen 518107, China
- Publication Type:Research Article
- Keywords:
H3N2 subtype influenza virus;
HA gene;
NA gene;
Molecular evolution;
Sequence analysis
- From:
Chinese Journal of Disease Control & Prevention
2019;23(9):1114-1120
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the molecular evolution of the Hemagglutinin (HA) and Neuraminidase (NA) genes of influenza A/H3N2 viruses in Shenzhen in the first half of 2017, so as to provide scientific basis for predicating influenza epidemic and variation. Methods A total of 40 influenza A/H3N2 viruses strains were selected and the molecular phylogenetic trees were constructed by bioinformatics software DNAStar, MEGA 7.0, etc. Then, the genetic characteristics and variation of HA and NA genes along with corresponding amino acids were analyzed. Results The homology of Shenzhen isolates reached 97.8%-100.0%, which located in the human-derived branch of Asia and North America. Compared with the vaccine strains A/Switzerland/9715293/2013(H3N2) and A/Hong Kong 14801/2014(H3N2) recommended by world Health Oraganication (WHO), there was a higher sequence similarity. Compared with the vaccine strain, HA and NA proteins had a number of amino acid sites replaced, of which HA 6 antigen sites and 2 receptor binding sites change; NA had a mutation of D151N/G located in enzyme activity sites. Potential N-glycosylation sites for HA and NA also changed. Conclusions The influenza A/H3N2 viruses in Shenzhen in the first half of 2017 has not yet formed a new subtype in the epidemic. Currently, the recommended vaccine strains still have some protective effects on the population. The replacement mutation of multiple amino acids sites of HA and NA suggests that the dynamic monitoring of molecular level of influenza A/H3N2 viruses need to be strengthened.
