The 2009 human pandemic influenza (H1N1) virus possesses the HA gene of the H1 subtype. The evolutionary process of the 2009 H1N1 virus remains to be defined. We performed genetic analyses of the HA gene by comparing the 2009 H1N1 virus with seasonal human and swine viruses. We analyzed sequences of 116 2009 H1N1 viruses, and obtained 1457 seasonal H1N1, 365 swine H1, and 1332 2009 H1N1 viruses from the database. Selection pressure for the 2009 H1N1 virus was higher than that for the swine virus and equivalent to that for the seasonal virus. Positions 206 and 264 were found to be positively selected sites. We also identified sites under different selection pressures from the seasonal or swine virus that may be involved in imparting significant biological characteristics. The evolutionary characteristics of the H1 gene of the 2009 H1N1 virus differed from those of seasonal and swine viruses.
This study revealed that viral etiology plays a significant role in the severity of the present ARI and that viral infection affects the host's susceptibility to subsequent ARIs.
Analyzing the evolutionary pattern of the influenza A(H1N1)pdm09 strain in different regions is important for understanding its diversification. We therefore conducted this study to elucidate the genetic variability and molecular evolution of the influenza A(H1N1)pdm09 strains that cir- .5 9 10 -3 and 1.6 9 10 -3 substitutions per site per year, respectively. Phylogenetic tree analysis demonstrated that Sendai isolates were clustered into global clade 7, which is characterized by an S203T mutation in the HA1 gene. Moreover, two distinct circulation clusters were present in the 2010-2011 season. Mutations were present in antigenic or receptor-binding domains of the HA1 segment, including A141V, S143G, S183P, S185T, and S203T. The Bayesian skyline plot model illustrated a steady rate for the maintenance of genetic diversity, followed by a slight increase in the later part of the 2010-2011 season. Selection analysis revealed that the HA1 (position 197) and NA (position 46) sites were under positive selection; however, no known mutation conferring resistance to NA inhibitors such as H275Y was observed. The effect on control of the influenza A(H1N1)pdm09 virus, including vaccine strain selection, requires continuous monitoring of the strain by genetic surveillance.
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