Genetic evolution of the neuraminidase of influenza A (H3N2) viruses from 1968 to 2009 and its correspondence to haemagglutinin evolution

Each year, influenza viruses cause epidemics by evading pre-existing humoral immunity through mutations in the major glycoproteins: the haemagglutinin (HA) and the neuraminidase (NA). In 2004, the antigenic evolution of HA of human influenza A (H3N2) viruses was mapped (Smith et al., Science 305, 37...

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Bibliographic Details
Published in:Journal of general virology 2012-09, Vol.93 (Pt 9), p.1996-2007
Main Authors: WESTGEEST, Kim B, DE GRAAF, Miranda, SMITH, Gavin J. D, SMITH, Derek J, FOUCHIER, Ron A. M, FOURMENT, Mathieu, BESTEBROER, Theo M, BEEK, Ruud Van, SPRONKEN, Monique I. J, DE JONG, Jan C, RIMMELZWAAN, Guus F, RUSSELL, Colin A, OSTERHAUS, Albert D. M. E
Format: Article
Language:English
Subjects:
Animal
Biological and medical sciences
Evolution, Molecular
Fundamental and applied biological sciences. Psychology
Genetics
Hemagglutinin Glycoproteins, Influenza Virus - genetics
Humans
Influenza A Virus, H3N2 Subtype - classification
Influenza A Virus, H3N2 Subtype - enzymology
Influenza A Virus, H3N2 Subtype - genetics
Influenza, Human - virology
Microbiology
Miscellaneous
Molecular Sequence Data
Mutation Rate
Neuraminidase - genetics
Phylogeny
Recombination, Genetic
Selection, Genetic
Viral Proteins - genetics
Virology
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Summary:Each year, influenza viruses cause epidemics by evading pre-existing humoral immunity through mutations in the major glycoproteins: the haemagglutinin (HA) and the neuraminidase (NA). In 2004, the antigenic evolution of HA of human influenza A (H3N2) viruses was mapped (Smith et al., Science 305, 371-376, 2004) from its introduction in humans in 1968 until 2003. The current study focused on the genetic evolution of NA and compared it with HA using the dataset of Smith and colleagues, updated to the epidemic of the 2009/2010 season. Phylogenetic trees and genetic maps were constructed to visualize the genetic evolution of NA and HA. The results revealed multiple reassortment events over the years. Overall rates of evolutionary change were lower for NA than for HA1 at the nucleotide level. Selection pressures were estimated, revealing an abundance of negatively selected sites and sparse positively selected sites. The differences found between the evolution of NA and HA1 warrant further analysis of the evolution of NA at the phenotypic level, as has been done previously for HA.
ISSN:0022-1317
1465-2099
1465-2099
DOI:10.1099/vir.0.043059-0