Genetic Variation in Neuraminidase Genes of Influenza A (H3N2) Viruses
Identifieur interne : 000159 ( 1968/Analysis ); précédent : 000158; suivant : 000160Genetic Variation in Neuraminidase Genes of Influenza A (H3N2) Viruses
Auteurs : Xiyan Xu ; Nancy J. Cox ; Catherine A. Bender ; Helen L. Regnery ; Michael W. ShawSource :
- Virology [ 0042-6822 ] ; 1996.
English descriptors
- Teeft :
- Academic press, Additional glycosylation site, Amino, Amino acid region, Amino acid residues, Amino acid sequences, Amino acid substitutions, Amino acids, Antigenic, Antigenic analysis, Antigenic drift, Antigenic sites, Antigenic variants, Antigenic variation, Appropriate vaccine strains, Branch points, Cell surface, Coding region, Disease control, Distinct lineages, Dnaml program, Entire coding region, Enzyme activity, Epidemic strains, Estimate phylogenies, Evolutionary pattern, Evolutionary tree, Field strains, Full strain designation, Gene, Gene sequences, Genetic reassortment, Genetic variation, Glycosylation, Hemagglutinin, Hemagglutinin genes, High variability, Horizontal lines, Human influenza, Influenza, Influenza season, Influenza states, Influenza type, Influenza vaccine, Influenza virus, Influenza virus hemagglutinin, Influenza virus neuraminidase, Influenza viruses, Kendal, Laver, Lineage, Linear regression analysis, Molecular epidemiology, Mutation rate, Mutational distances, Neuraminidase, Neuraminidase gene, Nucleotide, Nucleotide differences, Nucleotide sequences, Palese, Phylogenetic analysis, Phylogeny inference package, Plenum press, Potential glycosylation sites, Previous studies, Recent influenza, Reference strain, Same subtype, Sequence analysis software package, Sequence data, Substitution, Substrate binding pocket, Unpublished data, Vaccine, Vaccine strain selection, Vaccine strains, Vertical lines, Viral entry, Viras, Virol, Virology, Virology evolution, Virus, Virus evolution, Virus neuraminidase, Virus strains, Weekly epidemiol, Wisconsin genetics computer group, World health organization.
Abstract
Abstract: Nucleotide sequences of the neuraminidase (NA) genes of 33 influenza A (H3N2) epidemic strains isolated between 1968 and 1995 were analyzed to determine their evolutionary relationships. Phylogenetic analysis using the DNA maximum-likelihood method indicates that the NA genes of recent H3N2 field strains, like their hemagglutinin genes (HA), have evolved as two distinct lineages represented by the vaccine strains, A/Beijing/353/89 and A/Beijing/32/92 (or A/Shanghai/24/90). Furthermore, genetic reassortment of NA genes between the two lineages occurred during their circulation. Genetic reassortants, which bear an A/Beijing/32/92-like HA and an A/Beijing/353/89-like NA, have circulated worldwide and are representative of current influenza A (H3N2) epidemic strains. The mutation rate of the NA gene was found to be 2.28 × 10−3per nucleotide site per year with 42% of the mutations resulting in amino acid substitutions. Thirty-five percent of the amino acid substitutions was located in sites previously suggested to be reactive to antibody. Amino acid residues involved in NA enzyme activity have been conserved. Seven potential glycosylation sites identified in the NA of A/Hong Kong/8/68 virus were conserved by the majority of isolates, with more recently circulating viruses having an additional glycosylation site. Comparison of the rate of amino acid substitutions in the NA stalk to that of entire NA revealed high variability in this region. These findings demonstrate the importance of closely monitoring both the HA and the NA genes of influenza viruses to aid vaccine strain selection.
Url:
DOI: 10.1006/viro.1996.0519
Affiliations:
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Cox</name><affiliation><wicri:noCountry code="subField">30333</wicri:noCountry></affiliation></author><author><name sortKey="Bender, Catherine A" sort="Bender, Catherine A" uniqKey="Bender C" first="Catherine A." last="Bender">Catherine A. Bender</name><affiliation><wicri:noCountry code="subField">30333</wicri:noCountry></affiliation></author><author><name sortKey="Regnery, Helen L" sort="Regnery, Helen L" uniqKey="Regnery H" first="Helen L." last="Regnery">Helen L. Regnery</name><affiliation><wicri:noCountry code="subField">30333</wicri:noCountry></affiliation></author><author><name sortKey="Shaw, Michael W" sort="Shaw, Michael W" uniqKey="Shaw M" first="Michael W." last="Shaw">Michael W. Shaw</name><affiliation><wicri:noCountry code="subField">30333</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="ISSN">0042-6822</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996">1996</date><biblScope unit="volume">224</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="175">175</biblScope><biblScope unit="page" to="183">183</biblScope></imprint><idno type="ISSN">0042-6822</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0042-6822</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Academic press</term><term>Additional glycosylation site</term><term>Amino</term><term>Amino acid region</term><term>Amino acid residues</term><term>Amino acid sequences</term><term>Amino acid substitutions</term><term>Amino acids</term><term>Antigenic</term><term>Antigenic analysis</term><term>Antigenic drift</term><term>Antigenic sites</term><term>Antigenic variants</term><term>Antigenic variation</term><term>Appropriate vaccine strains</term><term>Branch points</term><term>Cell surface</term><term>Coding region</term><term>Disease control</term><term>Distinct lineages</term><term>Dnaml program</term><term>Entire coding region</term><term>Enzyme activity</term><term>Epidemic strains</term><term>Estimate phylogenies</term><term>Evolutionary pattern</term><term>Evolutionary tree</term><term>Field strains</term><term>Full strain designation</term><term>Gene</term><term>Gene sequences</term><term>Genetic reassortment</term><term>Genetic variation</term><term>Glycosylation</term><term>Hemagglutinin</term><term>Hemagglutinin genes</term><term>High variability</term><term>Horizontal lines</term><term>Human influenza</term><term>Influenza</term><term>Influenza season</term><term>Influenza states</term><term>Influenza type</term><term>Influenza vaccine</term><term>Influenza virus</term><term>Influenza virus hemagglutinin</term><term>Influenza virus neuraminidase</term><term>Influenza viruses</term><term>Kendal</term><term>Laver</term><term>Lineage</term><term>Linear regression analysis</term><term>Molecular epidemiology</term><term>Mutation rate</term><term>Mutational distances</term><term>Neuraminidase</term><term>Neuraminidase gene</term><term>Nucleotide</term><term>Nucleotide differences</term><term>Nucleotide sequences</term><term>Palese</term><term>Phylogenetic analysis</term><term>Phylogeny inference package</term><term>Plenum press</term><term>Potential glycosylation sites</term><term>Previous studies</term><term>Recent influenza</term><term>Reference strain</term><term>Same subtype</term><term>Sequence analysis software package</term><term>Sequence data</term><term>Substitution</term><term>Substrate binding pocket</term><term>Unpublished data</term><term>Vaccine</term><term>Vaccine strain selection</term><term>Vaccine strains</term><term>Vertical lines</term><term>Viral entry</term><term>Viras</term><term>Virol</term><term>Virology</term><term>Virology evolution</term><term>Virus</term><term>Virus evolution</term><term>Virus neuraminidase</term><term>Virus strains</term><term>Weekly epidemiol</term><term>Wisconsin genetics computer group</term><term>World health organization</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Nucleotide sequences of the neuraminidase (NA) genes of 33 influenza A (H3N2) epidemic strains isolated between 1968 and 1995 were analyzed to determine their evolutionary relationships. Phylogenetic analysis using the DNA maximum-likelihood method indicates that the NA genes of recent H3N2 field strains, like their hemagglutinin genes (HA), have evolved as two distinct lineages represented by the vaccine strains, A/Beijing/353/89 and A/Beijing/32/92 (or A/Shanghai/24/90). Furthermore, genetic reassortment of NA genes between the two lineages occurred during their circulation. Genetic reassortants, which bear an A/Beijing/32/92-like HA and an A/Beijing/353/89-like NA, have circulated worldwide and are representative of current influenza A (H3N2) epidemic strains. The mutation rate of the NA gene was found to be 2.28 × 10−3per nucleotide site per year with 42% of the mutations resulting in amino acid substitutions. Thirty-five percent of the amino acid substitutions was located in sites previously suggested to be reactive to antibody. Amino acid residues involved in NA enzyme activity have been conserved. Seven potential glycosylation sites identified in the NA of A/Hong Kong/8/68 virus were conserved by the majority of isolates, with more recently circulating viruses having an additional glycosylation site. Comparison of the rate of amino acid substitutions in the NA stalk to that of entire NA revealed high variability in this region. These findings demonstrate the importance of closely monitoring both the HA and the NA genes of influenza viruses to aid vaccine strain selection.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Bender, Catherine A" sort="Bender, Catherine A" uniqKey="Bender C" first="Catherine A." last="Bender">Catherine A. Bender</name><name sortKey="Cox, Nancy J" sort="Cox, Nancy J" uniqKey="Cox N" first="Nancy J." last="Cox">Nancy J. Cox</name><name sortKey="Regnery, Helen L" sort="Regnery, Helen L" uniqKey="Regnery H" first="Helen L." last="Regnery">Helen L. Regnery</name><name sortKey="Shaw, Michael W" sort="Shaw, Michael W" uniqKey="Shaw M" first="Michael W." last="Shaw">Michael W. Shaw</name><name sortKey="Xu, Xiyan" sort="Xu, Xiyan" uniqKey="Xu X" first="Xiyan" last="Xu">Xiyan Xu</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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