Genetic Variation in Neuraminidase Genes of Influenza A (H3N2) Viruses
Identifieur interne : 000B96 ( Istex/Corpus ); précédent : 000B95; suivant : 000B97Genetic 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strain, Same subtype, Sequence analysis software package, Sequence data, Substitution, Substrate binding pocket, Unpublished data, Vaccine, Vaccine strain selection, Vaccine strains, Vertical lines, Viral entry, Viras, Virol, Virology, Virology evolution, Virus, Virus evolution,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
Links to Exploration step
ISTEX:4514855D048EEE27613D8491E8982DB30654A3DALe document en format XML
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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><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>neuraminidase</json:string><json:string>antigenic</json:string><json:string>influenza</json:string><json:string>virology</json:string><json:string>virol</json:string><json:string>hemagglutinin</json:string><json:string>amino</json:string><json:string>laver</json:string><json:string>viras</json:string><json:string>glycosylation</json:string><json:string>kendal</json:string><json:string>influenza viruses</json:string><json:string>nucleotide sequences</json:string><json:string>influenza virus</json:string><json:string>palese</json:string><json:string>vaccine</json:string><json:string>antigenic drift</json:string><json:string>epidemic strains</json:string><json:string>evolutionary tree</json:string><json:string>field strains</json:string><json:string>entire coding region</json:string><json:string>influenza season</json:string><json:string>disease control</json:string><json:string>coding region</json:string><json:string>neuraminidase gene</json:string><json:string>nucleotide</json:string><json:string>virus</json:string><json:string>phylogenetic analysis</json:string><json:string>influenza type</json:string><json:string>amino acids</json:string><json:string>amino acid substitutions</json:string><json:string>virology evolution</json:string><json:string>potential glycosylation sites</json:string><json:string>amino acid sequences</json:string><json:string>sequence analysis software package</json:string><json:string>antigenic sites</json:string><json:string>vaccine strains</json:string><json:string>antigenic variants</json:string><json:string>genetic variation</json:string><json:string>influenza vaccine</json:string><json:string>estimate phylogenies</json:string><json:string>previous studies</json:string><json:string>antigenic analysis</json:string><json:string>academic press</json:string><json:string>gene</json:string><json:string>lineage</json:string><json:string>substitution</json:string><json:string>viral entry</json:string><json:string>weekly epidemiol</json:string><json:string>phylogeny inference package</json:string><json:string>amino acid residues</json:string><json:string>enzyme activity</json:string><json:string>unpublished data</json:string><json:string>reference strain</json:string><json:string>molecular epidemiology</json:string><json:string>cell surface</json:string><json:string>genetic reassortment</json:string><json:string>gene sequences</json:string><json:string>sequence data</json:string><json:string>wisconsin genetics computer group</json:string><json:string>dnaml program</json:string><json:string>horizontal lines</json:string><json:string>nucleotide differences</json:string><json:string>branch points</json:string><json:string>vertical lines</json:string><json:string>mutational distances</json:string><json:string>full strain designation</json:string><json:string>mutation rate</json:string><json:string>recent influenza</json:string><json:string>additional glycosylation site</json:string><json:string>amino acid region</json:string><json:string>substrate binding pocket</json:string><json:string>linear regression analysis</json:string><json:string>appropriate vaccine strains</json:string><json:string>high variability</json:string><json:string>virus evolution</json:string><json:string>evolutionary pattern</json:string><json:string>human influenza</json:string><json:string>same subtype</json:string><json:string>distinct lineages</json:string><json:string>antigenic variation</json:string><json:string>influenza virus hemagglutinin</json:string><json:string>vaccine strain selection</json:string><json:string>hemagglutinin genes</json:string><json:string>virus neuraminidase</json:string><json:string>influenza states</json:string><json:string>influenza virus neuraminidase</json:string><json:string>plenum press</json:string><json:string>world health organization</json:string><json:string>virus strains</json:string></teeft></keywords><author><json:item><name>Xiyan Xu</name><affiliations><json:string>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</json:string></affiliations></json:item><json:item><name>Nancy J. Cox</name><affiliations><json:string>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</json:string></affiliations></json:item><json:item><name>Catherine A. Bender</name><affiliations><json:string>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</json:string></affiliations></json:item><json:item><name>Helen L. Regnery</name><affiliations><json:string>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</json:string></affiliations></json:item><json:item><name>Michael W. Shaw</name><affiliations><json:string>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</json:string></affiliations></json:item></author><arkIstex>ark:/67375/6H6-L475B297-T</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><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.</abstract><qualityIndicators><refBibsNative>false</refBibsNative><abstractWordCount>235</abstractWordCount><abstractCharCount>1615</abstractCharCount><keywordCount>0</keywordCount><score>9.432</score><pdfWordCount>4612</pdfWordCount><pdfCharCount>30156</pdfCharCount><pdfVersion>1.1</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>532 x 711 pts</pdfPageSize></qualityIndicators><title>Genetic Variation in Neuraminidase Genes of Influenza A (H3N2) Viruses</title><pmid><json:string>8862412</json:string></pmid><pii><json:string>S0042-6822(96)90519-X</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Virology</title><language><json:string>unknown</json:string></language><publicationDate>1996</publicationDate><issn><json:string>0042-6822</json:string></issn><pii><json:string>S0042-6822(00)X0139-0</json:string></pii><volume>224</volume><issue>1</issue><pages><first>175</first><last>183</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1992</json:string><json:string>1968</json:string><json:string>1975</json:string><json:string>1993</json:string><json:string>09-06-96</json:string><json:string>1994</json:string><json:string>1983</json:string><json:string>1950</json:string><json:string>1990</json:string><json:string>1977</json:string><json:string>1989</json:string><json:string>1991</json:string><json:string>1978</json:string><json:string>1996</json:string><json:string>1985</json:string></date><geogName></geogName><orgName><json:string>Academic Press, Inc</json:string><json:string>China and Southern Asia</json:string><json:string>University of Wisconsin</json:string><json:string>China, South Asia</json:string><json:string>Biochem</json:string><json:string>University of Wisconsin Genetics Computer Group</json:string><json:string>National Center for Infectious Diseases, Centers for Disease Control and Prevention</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>J. Hyg</json:string><json:string>R. Krug</json:string><json:string>R. Wagner</json:string><json:string>Hong Kong</json:string><json:string>J. Virol</json:string><json:string>Blok</json:string><json:string>J. Epidemiol</json:string><json:string>Lynnette Brammer</json:string><json:string>J. Gen</json:string><json:string>H. Franenkel-Conrat</json:string><json:string>James Love</json:string><json:string>Air</json:string><json:string>Mark Hemphill</json:string><json:string>Nakao</json:string><json:string>C. Hannoun</json:string><json:string>Henrietta Hall</json:string></persName><placeName><json:string>Minneapolis</json:string><json:string>Foster City</json:string><json:string>SINGAPORE</json:string><json:string>United States</json:string><json:string>BEIJING</json:string><json:string>BANGKOK</json:string><json:string>Georgia</json:string><json:string>Madison</json:string><json:string>INDIA</json:string><json:string>China</json:string><json:string>Europe</json:string><json:string>HARBIN</json:string><json:string>America</json:string><json:string>YORK</json:string><json:string>CA</json:string><json:string>York</json:string><json:string>Postgrad</json:string><json:string>SAPPORO</json:string><json:string>JOHANNESBURG</json:string><json:string>WUHAN</json:string><json:string>NETHERLANDS</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>CDC, 1993</json:string><json:string>Castrucci and Kawaoka, 1993</json:string><json:string>Rota et al., 1990</json:string><json:string>Xu et al., 1993</json:string><json:string>Els et al., 1985</json:string><json:string>Phylip; Felsenstein, 1989</json:string><json:string>Air and Laver, 1989</json:string><json:string>Nakao et al., 1993</json:string><json:string>Tabak et al., 1982</json:string><json:string>Cox et al., 1989, 1993</json:string><json:string>Laver et al., 1982</json:string><json:string>Schild et al., 1983</json:string><json:string>Skehel et al., 1984</json:string><json:string>Devereaux et al., 1984</json:string><json:string>Kilbourne et al., 1968</json:string><json:string>Yamashita et al., 1988</json:string><json:string>Wilson et al., 1983</json:string><json:string>Both et al., 1983</json:string><json:string>Felsenstein, 1989</json:string><json:string>Cox et al., 1993</json:string><json:string>Skehel et al., 1983</json:string><json:string>Verhoeyen et al., 1980</json:string><json:string>Colman et al., 1983</json:string><json:string>Robertson et al., 1985</json:string><json:string>Kendal et al., 1979</json:string><json:string>Palese and Schulman, 1976</json:string><json:string>Li et al., 1992</json:string><json:string>Bean et al., 1992</json:string><json:string>Van Romput et al., 1982</json:string><json:string>Martinez et al., 1983</json:string><json:string>Rompuy et al., 1982</json:string><json:string>Hobson et al., 1972</json:string><json:string>Schulman, 1975</json:string><json:string>Nakajima et al., 1988</json:string><json:string>CDC, 1994</json:string><json:string>Rocha et al., 1991</json:string><json:string>Bentley and Brownlee, 1982</json:string><json:string>for review see Air and Laver, 1989</json:string><json:string>Blok and Air, 1980, 1982</json:string><json:string>Markoff and Lai, 1982</json:string><json:string>Lewis and Lai, 1982</json:string><json:string>Raymond et al., 1986</json:string><json:string>Cox and Bender, 1995</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-L475B297-T</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - virology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - virology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Virology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences biologiques fondamentales et appliquees. psychologie</json:string><json:string>4 - microbiologie</json:string></inist></categories><publicationDate>1996</publicationDate><copyrightDate>1996</copyrightDate><doi><json:string>10.1006/viro.1996.0519</json:string></doi><id>4514855D048EEE27613D8491E8982DB30654A3DA</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-L475B297-T/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-L475B297-T/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-L475B297-T/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Genetic Variation in Neuraminidase Genes of Influenza A (H3N2) Viruses</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©1996 Academic Press</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>1996</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note type="content">Section title: Regular Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Genetic Variation in Neuraminidase Genes of Influenza A (H3N2) Viruses</title><author xml:id="author-0000"><persName><forename type="first">Xiyan</forename><surname>Xu</surname></persName><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Nancy J.</forename><surname>Cox</surname></persName><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Catherine A.</forename><surname>Bender</surname></persName><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Helen L.</forename><surname>Regnery</surname></persName><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Michael W.</forename><surname>Shaw</surname></persName><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</affiliation></author><idno type="istex">4514855D048EEE27613D8491E8982DB30654A3DA</idno><idno type="ark">ark:/67375/6H6-L475B297-T</idno><idno type="DOI">10.1006/viro.1996.0519</idno><idno type="PII">S0042-6822(96)90519-X</idno></analytic><monogr><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="pISSN">0042-6822</idno><idno type="PII">S0042-6822(00)X0139-0</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="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></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1996</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>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.</p></abstract></profileDesc><revisionDesc><change when="1996">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-L475B297-T/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier converted-article found"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>YVIRO</jid><aid>90519</aid><ce:pii>S0042-6822(96)90519-X</ce:pii><ce:doi>10.1006/viro.1996.0519</ce:doi><ce:copyright type="full-transfer" year="1996">Academic Press</ce:copyright></item-info><head><ce:dochead><ce:textfn>Regular Article</ce:textfn></ce:dochead><ce:title>Genetic Variation in Neuraminidase Genes of Influenza A (H3N2) Viruses</ce:title><ce:author-group><ce:author><ce:given-name>Xiyan</ce:given-name><ce:surname>Xu</ce:surname><ce:cross-ref refid="FN1">1</ce:cross-ref></ce:author><ce:author><ce:given-name>Nancy J.</ce:given-name><ce:surname>Cox</ce:surname></ce:author><ce:author><ce:given-name>Catherine A.</ce:given-name><ce:surname>Bender</ce:surname></ce:author><ce:author><ce:given-name>Helen L.</ce:given-name><ce:surname>Regnery</ce:surname></ce:author><ce:author><ce:given-name>Michael W.</ce:given-name><ce:surname>Shaw</ce:surname></ce:author><ce:affiliation><ce:textfn>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</ce:textfn></ce:affiliation><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>To whom correspondence and reprint requests should be addressed. Fax: (404) 639-2334. E-mail: XXX1@CIDDVD1.em.cdc.gov.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="15" month="5" year="1996"></ce:date-received><ce:date-accepted day="29" month="7" year="1996"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>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<ce:sup>−3</ce:sup>per 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.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Genetic Variation in Neuraminidase Genes of Influenza A (H3N2) Viruses</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Genetic Variation in Neuraminidase Genes of Influenza A (H3N2) Viruses</title></titleInfo><name type="personal"><namePart type="given">Xiyan</namePart><namePart type="family">Xu</namePart><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</affiliation><description>To whom correspondence and reprint requests should be addressed. Fax: (404) 639-2334. E-mail: XXX1@CIDDVD1.em.cdc.gov.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nancy J.</namePart><namePart type="family">Cox</namePart><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Catherine A.</namePart><namePart type="family">Bender</namePart><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Helen L.</namePart><namePart type="family">Regnery</namePart><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael W.</namePart><namePart type="family">Shaw</namePart><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, 30333</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1996</dateIssued><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract 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.</abstract><note type="content">Section title: Regular Article</note><relatedItem type="host"><titleInfo><title>Virology</title></titleInfo><titleInfo type="abbreviated"><title>YVIRO</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1996</dateIssued></originInfo><identifier type="ISSN">0042-6822</identifier><identifier type="PII">S0042-6822(00)X0139-0</identifier><part><date>1996</date><detail type="volume"><number>224</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>356</end></extent><extent unit="pages"><start>175</start><end>183</end></extent></part></relatedItem><identifier type="istex">4514855D048EEE27613D8491E8982DB30654A3DA</identifier><identifier type="ark">ark:/67375/6H6-L475B297-T</identifier><identifier type="DOI">10.1006/viro.1996.0519</identifier><identifier type="PII">S0042-6822(96)90519-X</identifier><accessCondition type="use and reproduction" contentType="copyright">©1996 Academic Press</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Academic Press, ©1996</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-L475B297-T/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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