Prevalence, genetic drift of haemagglutinin, and antiviral resistance of influenza A/H3N2 viruses circulating in Shanghai in children during 2009–2012
Identifieur interne : 001899 ( Istex/Corpus ); précédent : 001898; suivant : 001900Prevalence, genetic drift of haemagglutinin, and antiviral resistance of influenza A/H3N2 viruses circulating in Shanghai in children during 2009–2012
Auteurs : Jiehao Cai ; Xiangshi Wang ; Baihui Zhao ; Weilei Yao ; Xiaohong Wang ; Qirong Zhu ; Mei ZengSource :
- Journal of Medical Virology [ 0146-6615 ] ; 2014-06.
Abstract
Influenza A/H3N2 viruses are associated with severe epidemics. Antiviral resistance and continued antigenic drift are the major concerns regarding prophylaxis and treatment of influenza. The objectives of this study were to investigate the prevalence and frequency of antiviral drug resistance in influenza A/H3N2 viruses circulating among Shanghainese children from June 2009 to May 2012 and to understand the genetic evolution of the hemagglutinin (HA) epitopes. Nasopharyngeal/throat swabs were collected from outpatients with influenza‐like illness. Of the 3,475 children tested, 344 (9.9%) were positive for influenza A/H3N2 viruses. Epidemics of influenza A/H3N2 occurred in July–September 2009, August 2010–January 2011, and November 2011–May 2012. The 71 A/H3N2‐positive specimens were sequenced to characterize the genotypic antiviral resistance and genetic drift in the HA epitopes. All of the 71 A/H3N2 viruses sequenced were genotypically resistant to adamantine but sensitive to oseltamivir. The HA1 sequence analysis revealed that the A/H3N2 viruses underwent constant mutations in the HA antigenic sites over the three seasons compared with the corresponding vaccine strains, and amino acid changes in at least three epitopes were observed each season. Phylogenic analyses indicated that the A/H3N2 strains circulating in Shanghai fell into clades different from those of the corresponding seasonal vaccine strains and were grouped into the A/Perth/16/2009 genetic clade and the A/Victoria/208/2009 genetic clades 3B, 3C, and 5. The continuous monitoring of genetic drift and antiviral resistance of influenza viruses is important for the management of influenza and for updating the vaccine composition. J. Med. Virol. 86:1026–1033, 2014. © 2014 Wiley Periodicals, Inc.
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DOI: 10.1002/jmv.23854
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ISTEX:6B14125E19F4BAD3A019AED8027F462D23A6DC7BLe document en format XML
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from="1026">1026</biblScope><biblScope unit="page" to="1033">1033</biblScope><biblScope unit="page-count">8</biblScope><date type="published" when="2014-06">2014-06</date></imprint><idno type="ISSN">0146-6615</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0146-6615</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Influenza A/H3N2 viruses are associated with severe epidemics. Antiviral resistance and continued antigenic drift are the major concerns regarding prophylaxis and treatment of influenza. The objectives of this study were to investigate the prevalence and frequency of antiviral drug resistance in influenza A/H3N2 viruses circulating among Shanghainese children from June 2009 to May 2012 and to understand the genetic evolution of the hemagglutinin (HA) epitopes. Nasopharyngeal/throat swabs were collected from outpatients with influenza‐like illness. Of the 3,475 children tested, 344 (9.9%) were positive for influenza A/H3N2 viruses. Epidemics of influenza A/H3N2 occurred in July–September 2009, August 2010–January 2011, and November 2011–May 2012. The 71 A/H3N2‐positive specimens were sequenced to characterize the genotypic antiviral resistance and genetic drift in the HA epitopes. All of the 71 A/H3N2 viruses sequenced were genotypically resistant to adamantine but sensitive to oseltamivir. The HA1 sequence analysis revealed that the A/H3N2 viruses underwent constant mutations in the HA antigenic sites over the three seasons compared with the corresponding vaccine strains, and amino acid changes in at least three epitopes were observed each season. Phylogenic analyses indicated that the A/H3N2 strains circulating in Shanghai fell into clades different from those of the corresponding seasonal vaccine strains and were grouped into the A/Perth/16/2009 genetic clade and the A/Victoria/208/2009 genetic clades 3B, 3C, and 5. The continuous monitoring of genetic drift and antiviral resistance of influenza viruses is important for the management of influenza and for updating the vaccine composition. J. Med. 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Antiviral resistance and continued antigenic drift are the major concerns regarding prophylaxis and treatment of influenza. The objectives of this study were to investigate the prevalence and frequency of antiviral drug resistance in influenza A/H3N2 viruses circulating among Shanghainese children from June 2009 to May 2012 and to understand the genetic evolution of the hemagglutinin (HA) epitopes. Nasopharyngeal/throat swabs were collected from outpatients with influenza‐like illness. Of the 3,475 children tested, 344 (9.9%) were positive for influenza A/H3N2 viruses. Epidemics of influenza A/H3N2 occurred in July–September 2009, August 2010–January 2011, and November 2011–May 2012. The 71 A/H3N2‐positive specimens were sequenced to characterize the genotypic antiviral resistance and genetic drift in the HA epitopes. All of the 71 A/H3N2 viruses sequenced were genotypically resistant to adamantine but sensitive to oseltamivir. The HA1 sequence analysis revealed that the A/H3N2 viruses underwent constant mutations in the HA antigenic sites over the three seasons compared with the corresponding vaccine strains, and amino acid changes in at least three epitopes were observed each season. Phylogenic analyses indicated that the A/H3N2 strains circulating in Shanghai fell into clades different from those of the corresponding seasonal vaccine strains and were grouped into the A/Perth/16/2009 genetic clade and the A/Victoria/208/2009 genetic clades 3B, 3C, and 5. The continuous monitoring of genetic drift and antiviral resistance of influenza viruses is important for the management of influenza and for updating the vaccine composition. J. Med. 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The 71 A/H3N2‐positive specimens were sequenced to characterize the genotypic antiviral resistance and genetic drift in the HA epitopes. All of the 71 A/H3N2 viruses sequenced were genotypically resistant to adamantine but sensitive to oseltamivir. The HA1 sequence analysis revealed that the A/H3N2 viruses underwent constant mutations in the HA antigenic sites over the three seasons compared with the corresponding vaccine strains, and amino acid changes in at least three epitopes were observed each season. Phylogenic analyses indicated that the A/H3N2 strains circulating in Shanghai fell into clades different from those of the corresponding seasonal vaccine strains and were grouped into the A/Perth/16/2009 genetic clade and the A/Victoria/208/2009 genetic clades 3B, 3C, and 5. 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Virol. 86:1026–1033, 2014</hi>.</hi> © 2014 Wiley Periodicals, Inc.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="jmv23854-kwd-0001">influenza A/H3N2 viruses</term><term xml:id="jmv23854-kwd-0002">hemagglutinin (HA)</term><term xml:id="jmv23854-kwd-0003">antiviral‐resistance</term><term xml:id="jmv23854-kwd-0004">Shanghai</term></keywords><keywords rend="articleCategory"><term>Research Article</term></keywords><keywords rend="tocHeading1"><term>Research Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-4GXCFGQ5-W/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" xml:lang="en" type="serialArticle" xml:id="jmv23854"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1002/(ISSN)1096-9071</doi><issn type="print">0146-6615</issn><issn type="electronic">1096-9071</issn><idGroup><id type="product" value="JMV"></id></idGroup><titleGroup><title type="main" sort="JOURNAL OF MEDICAL VIROLOGY">Journal of Medical Virology</title><title type="short">J. 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Virol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="60"><doi registered="yes">10.1002/jmv.v86.6</doi><copyright ownership="publisher">© 2014 Wiley Periodicals, Inc.</copyright><numberingGroup><numbering type="journalVolume" number="86">86</numbering><numbering type="journalIssue">6</numbering></numberingGroup><coverDate startDate="2014-06">June 2014</coverDate></publicationMeta><publicationMeta level="unit" position="170" type="article" status="forIssue"><doi>10.1002/jmv.23854</doi><idGroup><id type="unit" value="JMV23854"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="publisher">© 2014 Wiley Periodicals, Inc.</copyright><eventGroup><event type="manuscriptAccepted" date="2013-10-25"></event><event type="xmlCreated" agent="Thomson Digital" date="2014-02-12"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.3.0 mode:FullText" date="2014-04-28"></event><event type="publishedOnlineEarlyUnpaginated" date="2014-02-13"></event><event type="publishedOnlineFinalForm" date="2014-04-05"></event><event type="firstOnline" date="2014-02-13"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.6.4 mode:FullText" date="2015-10-07"></event></eventGroup><numberingGroup><numbering type="pageFirst">1026</numbering><numbering type="pageLast">1033</numbering></numberingGroup><correspondenceTo><lineatedText><line>Correspondence to: Mei Zeng, Department of Infectious Diseases, Children's Hospital of Fudan University, 399 Wanyuan Road, Shanghai 201102, China.</line><line>E‐mail:
<email>zengmeigao@aliyun.com</email></line></lineatedText></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JMV.JMV23854.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Prevalence, genetic drift of haemagglutinin, and antiviral resistance of influenza A/H3N2 viruses circulating in Shanghai in children during 2009–2012</title><title type="short">Influenza A/H3N2 Virus</title><title type="shortAuthors">Cai et al.</title></titleGroup><creators><creator xml:id="jmv23854-cr-0001" creatorRole="author" affiliationRef="#jmv23854-aff-0001"><personName><givenNames>Jiehao</givenNames> <familyName>Cai</familyName></personName></creator><creator xml:id="jmv23854-cr-0002" creatorRole="author" affiliationRef="#jmv23854-aff-0001"><personName><givenNames>Xiangshi</givenNames> <familyName>Wang</familyName></personName></creator><creator xml:id="jmv23854-cr-0003" creatorRole="author" affiliationRef="#jmv23854-aff-0002"><personName><givenNames>Baihui</givenNames> <familyName>Zhao</familyName></personName></creator><creator xml:id="jmv23854-cr-0004" creatorRole="author" affiliationRef="#jmv23854-aff-0001"><personName><givenNames>Weilei</givenNames> <familyName>Yao</familyName></personName></creator><creator xml:id="jmv23854-cr-0005" creatorRole="author" affiliationRef="#jmv23854-aff-0001"><personName><givenNames>Xiaohong</givenNames> <familyName>Wang</familyName></personName></creator><creator xml:id="jmv23854-cr-0006" creatorRole="author" affiliationRef="#jmv23854-aff-0001"><personName><givenNames>Qirong</givenNames> <familyName>Zhu</familyName></personName></creator><creator xml:id="jmv23854-cr-0007" creatorRole="author" affiliationRef="#jmv23854-aff-0001" corresponding="yes"><personName><givenNames>Mei</givenNames> <familyName>Zeng</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="jmv23854-aff-0001" countryCode="CN"><orgDiv>Department of Infectious Diseases</orgDiv><orgName>Children's Hospital of Fudan University</orgName><address><city>Shanghai</city><country>China</country></address></affiliation><affiliation xml:id="jmv23854-aff-0002" countryCode="CN"><orgDiv>Microbiology Department</orgDiv><orgName>Shanghai Municipal Center for Disease Control and Prevention</orgName><address><city>Shanghai</city><country>China</country></address></affiliation></affiliationGroup><keywordGroup type="author" xml:lang="en"><keyword xml:id="jmv23854-kwd-0001">influenza A/H3N2 viruses</keyword><keyword xml:id="jmv23854-kwd-0002">hemagglutinin (HA)</keyword><keyword xml:id="jmv23854-kwd-0003">antiviral‐resistance</keyword><keyword xml:id="jmv23854-kwd-0004">Shanghai</keyword></keywordGroup><fundingInfo><fundingAgency>Forgarty Research Training Award</fundingAgency><fundingNumber>TW005741‐07</fundingNumber></fundingInfo><abstractGroup><abstract type="main"><section xml:id="jmv23854-sec-0001"><p>Influenza A/H3N2 viruses are associated with severe epidemics. Antiviral resistance and continued antigenic drift are the major concerns regarding prophylaxis and treatment of influenza. The objectives of this study were to investigate the prevalence and frequency of antiviral drug resistance in influenza A/H3N2 viruses circulating among Shanghainese children from June 2009 to May 2012 and to understand the genetic evolution of the hemagglutinin (HA) epitopes. Nasopharyngeal/throat swabs were collected from outpatients with influenza‐like illness. Of the 3,475 children tested, 344 (9.9%) were positive for influenza A/H3N2 viruses. Epidemics of influenza A/H3N2 occurred in July–September 2009, August 2010–January 2011, and November 2011–May 2012. The 71 A/H3N2‐positive specimens were sequenced to characterize the genotypic antiviral resistance and genetic drift in the HA epitopes. All of the 71 A/H3N2 viruses sequenced were genotypically resistant to adamantine but sensitive to oseltamivir. The HA1 sequence analysis revealed that the A/H3N2 viruses underwent constant mutations in the HA antigenic sites over the three seasons compared with the corresponding vaccine strains, and amino acid changes in at least three epitopes were observed each season. Phylogenic analyses indicated that the A/H3N2 strains circulating in Shanghai fell into clades different from those of the corresponding seasonal vaccine strains and were grouped into the A/Perth/16/2009 genetic clade and the A/Victoria/208/2009 genetic clades 3B, 3C, and 5. The continuous monitoring of genetic drift and antiviral resistance of influenza viruses is important for the management of influenza and for updating the vaccine composition. <b><i>J. Med. Virol. 86:1026–1033, 2014</i>.</b> © 2014 Wiley Periodicals, Inc.</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="jmv23854-note-0001" numbered="no">Jiehao Cai and Xiangshi Wang joined the first author.</note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Prevalence, genetic drift of haemagglutinin, and antiviral resistance of influenza A/H3N2 viruses circulating in Shanghai in children during 2009–2012</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Influenza A/H3N2 Virus</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Prevalence, genetic drift of haemagglutinin, and antiviral resistance of influenza A/H3N2 viruses circulating in Shanghai in children during 2009–2012</title></titleInfo><name type="personal"><namePart type="given">Jiehao</namePart><namePart type="family">Cai</namePart><affiliation>Department of Infectious Diseases, Children's Hospital of Fudan University, Shanghai, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Xiangshi</namePart><namePart type="family">Wang</namePart><affiliation>Department of Infectious Diseases, Children's Hospital of Fudan University, Shanghai, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Baihui</namePart><namePart type="family">Zhao</namePart><affiliation>Microbiology Department, Shanghai Municipal Center for Disease Control and Prevention, Shanghai, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Weilei</namePart><namePart type="family">Yao</namePart><affiliation>Department of Infectious Diseases, Children's Hospital of Fudan University, Shanghai, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Xiaohong</namePart><namePart type="family">Wang</namePart><affiliation>Department of Infectious Diseases, Children's Hospital of Fudan University, Shanghai, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Qirong</namePart><namePart type="family">Zhu</namePart><affiliation>Department of Infectious Diseases, Children's Hospital of Fudan University, Shanghai, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mei</namePart><namePart type="family">Zeng</namePart><affiliation>Department of Infectious Diseases, Children's Hospital of Fudan University, Shanghai, China</affiliation><affiliation>Correspondence to: Mei Zeng, Department of Infectious Diseases, Children's Hospital of Fudan University, 399 Wanyuan Road, Shanghai 201102, China.E‐mail:</affiliation><affiliation>E-mail: zengmeigao@aliyun.com</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2014-06</dateIssued><dateCreated encoding="w3cdtf">2014-02-12</dateCreated><dateValid encoding="w3cdtf">2013-10-25</dateValid><copyrightDate encoding="w3cdtf">2014</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Influenza A/H3N2 viruses are associated with severe epidemics. Antiviral resistance and continued antigenic drift are the major concerns regarding prophylaxis and treatment of influenza. The objectives of this study were to investigate the prevalence and frequency of antiviral drug resistance in influenza A/H3N2 viruses circulating among Shanghainese children from June 2009 to May 2012 and to understand the genetic evolution of the hemagglutinin (HA) epitopes. Nasopharyngeal/throat swabs were collected from outpatients with influenza‐like illness. Of the 3,475 children tested, 344 (9.9%) were positive for influenza A/H3N2 viruses. Epidemics of influenza A/H3N2 occurred in July–September 2009, August 2010–January 2011, and November 2011–May 2012. The 71 A/H3N2‐positive specimens were sequenced to characterize the genotypic antiviral resistance and genetic drift in the HA epitopes. All of the 71 A/H3N2 viruses sequenced were genotypically resistant to adamantine but sensitive to oseltamivir. The HA1 sequence analysis revealed that the A/H3N2 viruses underwent constant mutations in the HA antigenic sites over the three seasons compared with the corresponding vaccine strains, and amino acid changes in at least three epitopes were observed each season. Phylogenic analyses indicated that the A/H3N2 strains circulating in Shanghai fell into clades different from those of the corresponding seasonal vaccine strains and were grouped into the A/Perth/16/2009 genetic clade and the A/Victoria/208/2009 genetic clades 3B, 3C, and 5. The continuous monitoring of genetic drift and antiviral resistance of influenza viruses is important for the management of influenza and for updating the vaccine composition. J. Med. Virol. 86:1026–1033, 2014. © 2014 Wiley Periodicals, Inc.</abstract><note type="funding">Forgarty Research Training Award - No. TW005741‐07; </note><subject lang="en"><genre>keywords</genre><topic>influenza A/H3N2 viruses</topic><topic>hemagglutinin (HA)</topic><topic>antiviral‐resistance</topic><topic>Shanghai</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Medical Virology</title></titleInfo><titleInfo type="abbreviated"><title>J. Med. 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