Search

In this study, we investigated the molecular epidemiology and evolution of influenza viruses from patients infected during the 2013-2014 influenza season in Beijing. A phylogenetic analysis of the hemagglutinin (HA) and neuraminidase (NA) sequences of influenza A and B viruses from 18 patients (6 A(H1N1)pdm09, 4 H3N2, and 8 influenza B virus) was performed. Among the influenza A viruses, A(H1N1)pdm09 was the dominant subtype, whereas the B/Yamagata lineage was predominant for influenza B. The influenza B HA and NA strains in Beijing were dominated by reassortants derived from the Yamagata lineage and the Victoria lineage, respectively. All six A(H1N1)pdm09 strains fell into the 6B genetic group with amino acid substitutions D97N, S185T, K163Q, and A256T; the four H3N2 strains fell into genetic group 3C.3 with substitutions T128A, R142G, N145S, and V186G, and the eight influenza B strains were categorized into subgroup 3.1 and harbored an N217S mutation. Two new mutations (K180Q and G187E at the Sa and Ca antigenic sites of the H1 segment, respectively), which were not detected during the preceding influenza season, were identified. Mutations N131K, S165I, N181Y, and D212N in HA of influenza B mapped to the 120-loop, 150-loop, 160-loop, and 190-helix, respectively. Our results reveal the molecular epidemiology and phylogenetic characteristics of influenza viruses within a single geographic location and can have implications for vaccination selection in northern China. [ABSTRACT FROM AUTHOR]

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 1 month. 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. [ABSTRACT FROM AUTHOR]