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Molecular epidemiology and evolution of A(H1N1)pdm09 and H3N2 virus during winter 2012-2013 in Beijing, China.
Infect Genet Evol. 2014 Aug; 26:228-40.IG

Abstract

In order to evaluate the epidemiology of influenza A and its surface antigens (haemagglutinin [HA] and neuraminidase [NA]) for molecular epidemiology and evolution analysis during winter 2012-2013 in Beijing, China, we worked within the framework of the Chinese National Influenza Center and collected nasal swabs of patients presenting with influenza-like illness. We found that both A(H1N1)pdm09 (46.8%) and H3N2 (53.2%) viruses were the predominant strains during the 2012-2013 influenza epidemic. The peak phase started at the second week of 2013 and lasted about 1month. We obtained HA and NA sequences of viruses from 44 patients by using Sanger sequencing. None of the strains had the oseltamivir resistance site H274Y. Phylogenetic analysis of 29 A(H1N1)pdm09 viruses showed a genetic drift from the vaccine strain A/California/07/2009 with mutations (H155Q/R and L178I) at the antigenic sites Ca and Sa of HA; the strains were classified into genetic groups 6 and 7 because of the presence of D114N, S160G, S202T, and A214T mutations in HA. H3N2 viruses formed seasonal phylogenetic clusters representative for each season from 2000 to 2013; 15 of the 2012-2013 H3N2 strains were assigned to the A/Victoria/361/2011 genetic clade with mutations at the antigenic sites A, B and C of HA, including R158K/G, N161S, Q172H, and N294K; the 2012-2013 strains with V239I, S61N, T64I, and A214S HA mutations were classified into subgroup 3C. The mutation of potential N-linked glycosylation residues at the antigenic sites of HA and around the enzymatic active center of NA may have increased viral pathogenicity by masking antigenic sites from immune recognition. Our data suggest that influenza vaccines are generally effective, but still provide suboptimal protection due to antigenic variation. This study increases the understanding of influenza A viruses in humans and is informative for future vaccine strain selection.

Authors+Show Affiliations

Department of Infectious Disease, Peking University Hepatology Institute, Peking University People's Hospital, Beijing 100044, China.Department of Infectious Disease, Peking University Hepatology Institute, Peking University People's Hospital, Beijing 100044, China. Electronic address: gaoyan6384@163.com.Department of Infectious Disease, Peking University Hepatology Institute, Peking University People's Hospital, Beijing 100044, China.Department of Infectious Disease, Peking University Hepatology Institute, Peking University People's Hospital, Beijing 100044, China.Department of Infectious Disease, Peking University Hepatology Institute, Peking University People's Hospital, Beijing 100044, China.Department of Infectious Disease, The Third Affiliated Hospital of Zhongshan University, Guangzhou 510630, China.Department of Infectious Disease, Peking University Hepatology Institute, Peking University People's Hospital, Beijing 100044, China.

Pub Type(s)

Historical Article
Journal Article

Language

eng

PubMed ID

24911284

Citation

Fang, Qiongxuan, et al. "Molecular Epidemiology and Evolution of A(H1N1)pdm09 and H3N2 Virus During Winter 2012-2013 in Beijing, China." Infection, Genetics and Evolution : Journal of Molecular Epidemiology and Evolutionary Genetics in Infectious Diseases, vol. 26, 2014, pp. 228-40.
Fang Q, Gao Y, Chen M, et al. Molecular epidemiology and evolution of A(H1N1)pdm09 and H3N2 virus during winter 2012-2013 in Beijing, China. Infect Genet Evol. 2014;26:228-40.
Fang, Q., Gao, Y., Chen, M., Guo, X., Yang, X., Yang, X., & Wei, L. (2014). Molecular epidemiology and evolution of A(H1N1)pdm09 and H3N2 virus during winter 2012-2013 in Beijing, China. Infection, Genetics and Evolution : Journal of Molecular Epidemiology and Evolutionary Genetics in Infectious Diseases, 26, 228-40. https://doi.org/10.1016/j.meegid.2014.05.034
Fang Q, et al. Molecular Epidemiology and Evolution of A(H1N1)pdm09 and H3N2 Virus During Winter 2012-2013 in Beijing, China. Infect Genet Evol. 2014;26:228-40. PubMed PMID: 24911284.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Molecular epidemiology and evolution of A(H1N1)pdm09 and H3N2 virus during winter 2012-2013 in Beijing, China. AU - Fang,Qiongxuan, AU - Gao,Yan, AU - Chen,Meifang, AU - Guo,Xiaolin, AU - Yang,Xia, AU - Yang,Xiaohua, AU - Wei,Lai, Y1 - 2014/06/07/ PY - 2014/01/22/received PY - 2014/05/12/revised PY - 2014/05/30/accepted PY - 2014/6/10/entrez PY - 2014/6/10/pubmed PY - 2016/3/25/medline KW - A(H1N1)pdm09 KW - H3N2 KW - Molecular-genetic analysis KW - Phylogeny SP - 228 EP - 40 JF - Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases JO - Infect Genet Evol VL - 26 N2 - In order to evaluate the epidemiology of influenza A and its surface antigens (haemagglutinin [HA] and neuraminidase [NA]) for molecular epidemiology and evolution analysis during winter 2012-2013 in Beijing, China, we worked within the framework of the Chinese National Influenza Center and collected nasal swabs of patients presenting with influenza-like illness. We found that both A(H1N1)pdm09 (46.8%) and H3N2 (53.2%) viruses were the predominant strains during the 2012-2013 influenza epidemic. The peak phase started at the second week of 2013 and lasted about 1month. We obtained HA and NA sequences of viruses from 44 patients by using Sanger sequencing. None of the strains had the oseltamivir resistance site H274Y. Phylogenetic analysis of 29 A(H1N1)pdm09 viruses showed a genetic drift from the vaccine strain A/California/07/2009 with mutations (H155Q/R and L178I) at the antigenic sites Ca and Sa of HA; the strains were classified into genetic groups 6 and 7 because of the presence of D114N, S160G, S202T, and A214T mutations in HA. H3N2 viruses formed seasonal phylogenetic clusters representative for each season from 2000 to 2013; 15 of the 2012-2013 H3N2 strains were assigned to the A/Victoria/361/2011 genetic clade with mutations at the antigenic sites A, B and C of HA, including R158K/G, N161S, Q172H, and N294K; the 2012-2013 strains with V239I, S61N, T64I, and A214S HA mutations were classified into subgroup 3C. The mutation of potential N-linked glycosylation residues at the antigenic sites of HA and around the enzymatic active center of NA may have increased viral pathogenicity by masking antigenic sites from immune recognition. Our data suggest that influenza vaccines are generally effective, but still provide suboptimal protection due to antigenic variation. This study increases the understanding of influenza A viruses in humans and is informative for future vaccine strain selection. SN - 1567-7257 UR - https://www.unboundmedicine.com/medline/citation/24911284/Molecular_epidemiology_and_evolution_of_A_H1N1_pdm09_and_H3N2_virus_during_winter_2012_2013_in_Beijing_China_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1567-1348(14)00203-2 DB - PRIME DP - Unbound Medicine ER -