Distinct patterns of evolution between respiratory syncytial virus subgroups A and B From New Zealand isolates collected over thirty‐seven years
Identifieur interne : 004296 ( Main/Exploration ); précédent : 004295; suivant : 004297Distinct patterns of evolution between respiratory syncytial virus subgroups A and B From New Zealand isolates collected over thirty‐seven years
Auteurs : James W. Matheson [Nouvelle-Zélande] ; Fenella J. Rich [Nouvelle-Zélande] ; Catherine Cohet [Nouvelle-Zélande] ; Keith Grimwood [Nouvelle-Zélande] ; Q. Sue Huang [Nouvelle-Zélande] ; David Penny [Nouvelle-Zélande] ; Michael D. Hendy [Nouvelle-Zélande] ; Joanna R. Kirman [Nouvelle-Zélande]Source :
- Journal of Medical Virology [ 0146-6615 ] ; 2006-10.
English descriptors
- Teeft :
- Adenosine deaminases, Alignment, Amino, Amino acid change, Amino acid changes, Amino acid substitutions, Amino acid variability, Amino acids, Antigenic, Antigenic differences, Attachment protein, Base pairs, Branch lengths, Circulation patterns, Clin microbiol, Codon usage, Color coding, Consecutive seasons, Evolutionary pattern, Evolutionary patterns, Gene sequences, Genetic distances, Genetic diversity, Genetic variability, Genotype, Glycoprotein, Grant sponsor, Gray boxes, Greater percentage, Heuristic search, High number, Higher rate, Important cause, International alignments, International sequences, Majority consensus, Malaghan institute, Massey university, Maximum parsimony trees, Medical research, Melero, Molecular epidemiology, Molecular evolution, Multiple paths, Mutation, Mutation rate, Node, Nucleotide, Other countries, Parsimony, Phylogenetic, Phylogenetic analysis, Phylogenetic network, Previous studies, Primer, Proc natl acad, Product sizes, Protein alignment, Protein length, Reading frame, Reference strain, Representative sequence, Respiratory syncytial virus, Respiratory syncytial virus infection, Respiratory syncytial viruses, Respiratory tract infections, Risk factors, Roche diagnostics, Same data, Sample isolation, Sample size, Sampling bias, Selective pressure, Similar period, Subgroup, Subgroups exhibit, Subtypes, Sullender, Syncytial, Syncytial virus, Syncytial virus subgroup, Syncytial viruses, Time period, Tract infections, Variable regions, Venter, Viral, Viral attachment glycoprotein, Virol, Virus, Wellington, Wellington hospital, Zealand, Zealand alignments, Zealand infants, Zealand viruses, Zlateva.
Abstract
Respiratory syncytial virus (RSV) is the most important cause of viral lower respiratory tract infections in infants and children worldwide. In New Zealand, infants with RSV disease are hospitalized at a higher rate than other industrialized countries, without a proportionate increase in known risk factors. The molecular epidemiology of RSV in New Zealand has never been described. Therefore, we analyzed viral attachment glycoprotein (G) gene sequences from 106 RSV subgroup A isolates collected in New Zealand between 1967 and 2003, and 38 subgroup B viruses collected between 1984 and 2004. Subgroup A and B sequences were aligned separately, and compared to sequences of viruses isolated from other countries during a similar period. Genotyping and clustering analyses showed RSV in New Zealand is similar and temporally related to viruses found in other countries. By quantifying temporal clustering, we found subgroup B viruses clustered more strongly than subgroup A viruses. RSV B sequences displayed more variability in stop codon usage and predicted protein length, and had a higher degree of predicted O‐glycosylation site changes than RSV A. The mutation rate calculated for the RSV B G gene was significantly higher than for RSV A. Together, these data reveal that RSV subgroups exhibit different patterns of evolution, with subgroup B viruses evolving faster than A. J. Med. Virol. 78:1354–1364, 2006. © 2006 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jmv.20702
Affiliations:
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Box 7060, Wellington South</wicri:regionArea><wicri:noRegion>Wellington South</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Medical Virology</title><title level="j" type="alt">JOURNAL OF MEDICAL VIROLOGY</title><idno type="ISSN">0146-6615</idno><idno type="eISSN">1096-9071</idno><imprint><biblScope unit="vol">78</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1354">1354</biblScope><biblScope unit="page" to="1364">1364</biblScope><biblScope unit="page-count">11</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-10">2006-10</date></imprint><idno type="ISSN">0146-6615</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0146-6615</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Adenosine deaminases</term><term>Alignment</term><term>Amino</term><term>Amino acid change</term><term>Amino acid changes</term><term>Amino acid substitutions</term><term>Amino acid variability</term><term>Amino acids</term><term>Antigenic</term><term>Antigenic differences</term><term>Attachment protein</term><term>Base pairs</term><term>Branch lengths</term><term>Circulation patterns</term><term>Clin microbiol</term><term>Codon usage</term><term>Color coding</term><term>Consecutive seasons</term><term>Evolutionary pattern</term><term>Evolutionary patterns</term><term>Gene sequences</term><term>Genetic distances</term><term>Genetic diversity</term><term>Genetic variability</term><term>Genotype</term><term>Glycoprotein</term><term>Grant sponsor</term><term>Gray boxes</term><term>Greater percentage</term><term>Heuristic search</term><term>High number</term><term>Higher rate</term><term>Important cause</term><term>International alignments</term><term>International sequences</term><term>Majority consensus</term><term>Malaghan institute</term><term>Massey university</term><term>Maximum parsimony trees</term><term>Medical research</term><term>Melero</term><term>Molecular epidemiology</term><term>Molecular evolution</term><term>Multiple paths</term><term>Mutation</term><term>Mutation rate</term><term>Node</term><term>Nucleotide</term><term>Other countries</term><term>Parsimony</term><term>Phylogenetic</term><term>Phylogenetic analysis</term><term>Phylogenetic network</term><term>Previous studies</term><term>Primer</term><term>Proc natl acad</term><term>Product sizes</term><term>Protein alignment</term><term>Protein length</term><term>Reading frame</term><term>Reference strain</term><term>Representative sequence</term><term>Respiratory syncytial virus</term><term>Respiratory syncytial virus infection</term><term>Respiratory syncytial viruses</term><term>Respiratory tract infections</term><term>Risk factors</term><term>Roche diagnostics</term><term>Same data</term><term>Sample isolation</term><term>Sample size</term><term>Sampling bias</term><term>Selective pressure</term><term>Similar period</term><term>Subgroup</term><term>Subgroups exhibit</term><term>Subtypes</term><term>Sullender</term><term>Syncytial</term><term>Syncytial virus</term><term>Syncytial virus subgroup</term><term>Syncytial viruses</term><term>Time period</term><term>Tract infections</term><term>Variable regions</term><term>Venter</term><term>Viral</term><term>Viral attachment glycoprotein</term><term>Virol</term><term>Virus</term><term>Wellington</term><term>Wellington hospital</term><term>Zealand</term><term>Zealand alignments</term><term>Zealand infants</term><term>Zealand viruses</term><term>Zlateva</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Respiratory syncytial virus (RSV) is the most important cause of viral lower respiratory tract infections in infants and children worldwide. In New Zealand, infants with RSV disease are hospitalized at a higher rate than other industrialized countries, without a proportionate increase in known risk factors. The molecular epidemiology of RSV in New Zealand has never been described. Therefore, we analyzed viral attachment glycoprotein (G) gene sequences from 106 RSV subgroup A isolates collected in New Zealand between 1967 and 2003, and 38 subgroup B viruses collected between 1984 and 2004. Subgroup A and B sequences were aligned separately, and compared to sequences of viruses isolated from other countries during a similar period. Genotyping and clustering analyses showed RSV in New Zealand is similar and temporally related to viruses found in other countries. By quantifying temporal clustering, we found subgroup B viruses clustered more strongly than subgroup A viruses. RSV B sequences displayed more variability in stop codon usage and predicted protein length, and had a higher degree of predicted O‐glycosylation site changes than RSV A. The mutation rate calculated for the RSV B G gene was significantly higher than for RSV A. Together, these data reveal that RSV subgroups exhibit different patterns of evolution, with subgroup B viruses evolving faster than A. J. Med. Virol. 78:1354–1364, 2006. © 2006 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Nouvelle-Zélande</li></country></list><tree><country name="Nouvelle-Zélande"><noRegion><name sortKey="Matheson, James W" sort="Matheson, James W" uniqKey="Matheson J" first="James W." last="Matheson">James W. 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Kirman</name><name sortKey="Matheson, James W" sort="Matheson, James W" uniqKey="Matheson J" first="James W." last="Matheson">James W. Matheson</name><name sortKey="Penny, David" sort="Penny, David" uniqKey="Penny D" first="David" last="Penny">David Penny</name><name sortKey="Rich, Fenella J" sort="Rich, Fenella J" uniqKey="Rich F" first="Fenella J." last="Rich">Fenella J. Rich</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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