Abstract

BackgroundAnnual seasonal influenza outbreaks are associated with high morbidity and mortality.ObjectiveTo index and document evolutionary changes among influenza A H1N1 and H3N2 viruses isolated from Thailand during 2006–2009, using complete genome sequences.MethodsNasopharyngeal aspirates were collected from patients diagnosed with respiratory illness in Thailand during 2006–2009. All samples were screened for Influenza A virus. A total of 13 H1N1 and 21 H3N2 were confirmed and whole genome sequenced for the evolutionary analysis using standard phylogenetic approaches.ResultsPhylogenetic analysis of HA revealed a clear diversification of seasonal from vaccine strain lineages. H3N2 seasonal clusters were closely related to the WHO recommended vaccine strains in each season. Most H1N1 isolates could be differentiated into 3 lineages. The A/Brisbane/59/2007 lineage, a vaccine strain for H1N1 since 2008, is closely related with the H1N1 subtypes circulating in 2009. HA sequences were conserved at the receptor-binding site. Amino acid variations in the antigenic site resulted in a possible N-linked glycosylation motif. Recent H3N2 isolates had higher genetic variations compared to H1N1 isolates. Most substitutions in the NP protein were clustered in the T-cell recognition domains.ConclusionIn this study we performed evolutionary genetic analysis of influenza A viruses in Thailand between 2006–2009. Although the current vaccine strain is efficient for controlling the circulating outbreak subtypes, surveillance is necessary to provide unambiguous information on emergent viruses. In summary, the findings of this study contribute the understanding of evolution in influenza A viruses in humans and is useful for routine surveillance and vaccine strain selection.

Highlights

  • Influenza A viruses are negative-strand RNA viruses of the family Orthomyxoviridae which can be divided into subtypes based on the antigenic properties of the surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA) [1]

  • Global pandemics of influenza occur, infecting 20% to 40% of the population in a single year and dramatically raising death rates. Three such major global pandemics caused by novel antigenic variants of influenza viruses have affected the human population: in 1918 (H1N1 subtype), in 1957 (H2N2), and in 1968 (H3N2)

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Summary

Introduction

Influenza A viruses are negative-strand RNA viruses of the family Orthomyxoviridae which can be divided into subtypes based on the antigenic properties of the surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA) [1]. Influenza epidemics are associated with above average annual mortality levels, causing 10,000 to 15,000 deaths. Global pandemics of influenza occur, infecting 20% to 40% of the population in a single year and dramatically raising death rates. Three such major global pandemics caused by novel antigenic variants of influenza viruses have affected the human population: in 1918 (H1N1 subtype), in 1957 (H2N2), and in 1968 (H3N2). The novel H1N1 influenza virus that emerged in humans in Mexico in early 2009 and spread globally in the human population has been declared a pandemic strain. Annual seasonal influenza outbreaks are associated with high morbidity and mortality

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