Mouse lung‐adapted mutation of E190G in hemagglutinin from H5N1 influenza virus contributes to attenuation in mice
Identifieur interne : 000920 ( Istex/Corpus ); précédent : 000919; suivant : 000921Mouse lung‐adapted mutation of E190G in hemagglutinin from H5N1 influenza virus contributes to attenuation in mice
Auteurs : Pengfei Han ; Yi Hu ; Wei Sun ; Sen Zhang ; Yuchang Li ; Xiaoyan Wu ; Yinhui Yang ; Qingyu Zhu ; Tao Jiang ; Jing Li ; Chengfeng QinSource :
- Journal of Medical Virology [ 0146-6615 ] ; 2015-11.
Abstract
The highly pathogenic H5N1 avian influenza virus is one of the greatest influenza pandemic threats since 2003. The association of the receptor binding domain (RBD) with the virulence of influenza virus is rarely addressed, particularly of H5N1 influenza viruses. In this study, BALB/c mice were intranasally infected with A/Vietnam/1194/2004 (VN1194, H5N1). The mouse lung‐adapted variants were isolated and the mutation of E190G (H3 numbering) in the RBD was recognized. The recombinant virus, rVN‐E190G carrying E190G in hemagglutinin (HA) was designed and rescued using reverse genetics techniques. The receptor binding activity, growth curve and pathogenicity in mice of the rVN‐E190G were investigated. Results demonstrated that rVN‐E190G virus increased the binding avidity to α2,6 SA (sialic acid) and reduced the affinity to α2,3 SA, meanwhile weakened the viral replication in vitro. Moreover, the virulence assessment demonstrated that rVN‐E190G was attenuated in mice. These results indicated that the mutation E190G in HA decreases H5N1 viral replication in vitro and significantly attenuates virulence in vivo. These findings identify one of the determinants in RBD which can be associated with H5N1 virulence in mice. J. Med. Virol. 87:1816–1822, 2015. © 2015 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/jmv.24257
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E‐mail: (J. L.); (C. Q.)</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: lj-pbs@163.comqincf@bmi.ac.cn</mods:affiliation></affiliation></author><author><name sortKey="Qin, Chengfeng" sort="Qin, Chengfeng" uniqKey="Qin C" first="Chengfeng" last="Qin">Chengfeng Qin</name><affiliation><mods:affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence to: Jing Li and Chengfeng Qin, No. 20, Dongda Street, Fengtai District, Beijing 100071, PR China. E‐mail: (J. L.); (C. Q.)</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: lj-pbs@163.comqincf@bmi.ac.cn</mods:affiliation></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">87</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1816">1816</biblScope><biblScope unit="page" to="1822">1822</biblScope><biblScope unit="page-count">7</biblScope><date type="published" when="2015-11">2015-11</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" xml:lang="en">The highly pathogenic H5N1 avian influenza virus is one of the greatest influenza pandemic threats since 2003. The association of the receptor binding domain (RBD) with the virulence of influenza virus is rarely addressed, particularly of H5N1 influenza viruses. In this study, BALB/c mice were intranasally infected with A/Vietnam/1194/2004 (VN1194, H5N1). The mouse lung‐adapted variants were isolated and the mutation of E190G (H3 numbering) in the RBD was recognized. The recombinant virus, rVN‐E190G carrying E190G in hemagglutinin (HA) was designed and rescued using reverse genetics techniques. The receptor binding activity, growth curve and pathogenicity in mice of the rVN‐E190G were investigated. Results demonstrated that rVN‐E190G virus increased the binding avidity to α2,6 SA (sialic acid) and reduced the affinity to α2,3 SA, meanwhile weakened the viral replication in vitro. Moreover, the virulence assessment demonstrated that rVN‐E190G was attenuated in mice. These results indicated that the mutation E190G in HA decreases H5N1 viral replication in vitro and significantly attenuates virulence in vivo. These findings identify one of the determinants in RBD which can be associated with H5N1 virulence in mice. J. Med. Virol. 87:1816–1822, 2015. © 2015 Wiley Periodicals, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Pengfei Han</name><affiliations><json:string>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</json:string></affiliations></json:item><json:item><name>Yi Hu</name><affiliations><json:string>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</json:string></affiliations></json:item><json:item><name>Wei Sun</name><affiliations><json:string>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</json:string></affiliations></json:item><json:item><name>Sen Zhang</name><affiliations><json:string>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</json:string></affiliations></json:item><json:item><name>Yuchang Li</name><affiliations><json:string>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</json:string></affiliations></json:item><json:item><name>Xiaoyan Wu</name><affiliations><json:string>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</json:string></affiliations></json:item><json:item><name>Yinhui Yang</name><affiliations><json:string>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</json:string></affiliations></json:item><json:item><name>Qingyu Zhu</name><affiliations><json:string>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</json:string></affiliations></json:item><json:item><name>Tao jiang</name><affiliations><json:string>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</json:string></affiliations></json:item><json:item><name>Jing Li</name><affiliations><json:string>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</json:string><json:string>Correspondence to: Jing Li and Chengfeng Qin, No. 20, Dongda Street, Fengtai District, Beijing 100071, PR China. E‐mail: (J. L.); (C. Q.)</json:string><json:string>E-mail: lj-pbs@163.comqincf@bmi.ac.cn</json:string></affiliations></json:item><json:item><name>Chengfeng Qin</name><affiliations><json:string>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</json:string><json:string>Correspondence to: Jing Li and Chengfeng Qin, No. 20, Dongda Street, Fengtai District, Beijing 100071, PR China. E‐mail: (J. L.); (C. Q.)</json:string><json:string>E-mail: lj-pbs@163.comqincf@bmi.ac.cn</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>H5N1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hemagglutinin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>receptor binding domain</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mouse model</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>attenuation</value></json:item></subject><articleId><json:string>JMV24257</json:string></articleId><arkIstex>ark:/67375/WNG-8W33562B-J</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>The highly pathogenic H5N1 avian influenza virus is one of the greatest influenza pandemic threats since 2003. The association of the receptor binding domain (RBD) with the virulence of influenza virus is rarely addressed, particularly of H5N1 influenza viruses. In this study, BALB/c mice were intranasally infected with A/Vietnam/1194/2004 (VN1194, H5N1). The mouse lung‐adapted variants were isolated and the mutation of E190G (H3 numbering) in the RBD was recognized. The recombinant virus, rVN‐E190G carrying E190G in hemagglutinin (HA) was designed and rescued using reverse genetics techniques. The receptor binding activity, growth curve and pathogenicity in mice of the rVN‐E190G were investigated. Results demonstrated that rVN‐E190G virus increased the binding avidity to α2,6 SA (sialic acid) and reduced the affinity to α2,3 SA, meanwhile weakened the viral replication in vitro. Moreover, the virulence assessment demonstrated that rVN‐E190G was attenuated in mice. These results indicated that the mutation E190G in HA decreases H5N1 viral replication in vitro and significantly attenuates virulence in vivo. These findings identify one of the determinants in RBD which can be associated with H5N1 virulence in mice. J. Med. Virol. 87:1816–1822, 2015. © 2015 Wiley Periodicals, Inc.</abstract><qualityIndicators><score>8.891</score><pdfWordCount>4623</pdfWordCount><pdfCharCount>28075</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>593.972 x 792 pts</pdfPageSize><pdfWordsPerPage>660</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>189</abstractWordCount><abstractCharCount>1297</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Mouse lung‐adapted mutation of E190G in hemagglutinin from H5N1 influenza virus contributes to attenuation in mice</title><genre><json:string>article</json:string></genre><host><title>Journal of Medical 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Attenuation</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher ref="https://scientific-publisher.data.istex.fr/ark:/67375/H02-QW5Q88H5-V">Wiley Publishing Ltd</publisher><availability><licence>© 2015 Wiley Periodicals, Inc.</licence></availability><date type="published" when="2015-11"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Mouse lung‐adapted mutation of E190G in hemagglutinin from H5N1 influenza virus contributes to attenuation in mice</title><title level="a" type="short">E190G in HA of H5N1 Confer Attenuation</title><author xml:id="author-0000"><persName><forename type="first">Pengfei</forename><surname>Han</surname></persName><affiliation><orgName type="division">Department of Virology</orgName><orgName type="division">State Key Laboratory of Pathogens and Biosecurity</orgName><orgName type="institution">Beijing Institute of Microbiology and Epidemiology</orgName><address><settlement>Beijing</settlement><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Yi</forename><surname>Hu</surname></persName><affiliation><orgName type="division">Department of Virology</orgName><orgName type="division">State Key Laboratory of Pathogens and Biosecurity</orgName><orgName type="institution">Beijing Institute of Microbiology and Epidemiology</orgName><address><settlement>Beijing</settlement><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Wei</forename><surname>Sun</surname></persName><affiliation><orgName type="division">Department of Virology</orgName><orgName type="division">State Key Laboratory of Pathogens and Biosecurity</orgName><orgName type="institution">Beijing Institute of Microbiology and Epidemiology</orgName><address><settlement>Beijing</settlement><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Sen</forename><surname>Zhang</surname></persName><affiliation><orgName type="division">Department of Virology</orgName><orgName type="division">State Key Laboratory of Pathogens and Biosecurity</orgName><orgName type="institution">Beijing Institute of Microbiology and Epidemiology</orgName><address><settlement>Beijing</settlement><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Yuchang</forename><surname>Li</surname></persName><affiliation><orgName type="division">Department of Virology</orgName><orgName type="division">State Key Laboratory of Pathogens and Biosecurity</orgName><orgName type="institution">Beijing Institute of Microbiology and Epidemiology</orgName><address><settlement>Beijing</settlement><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Xiaoyan</forename><surname>Wu</surname></persName><affiliation><orgName type="division">Department of Virology</orgName><orgName type="division">State Key Laboratory of Pathogens and Biosecurity</orgName><orgName type="institution">Beijing Institute of Microbiology and Epidemiology</orgName><address><settlement>Beijing</settlement><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Yinhui</forename><surname>Yang</surname></persName><affiliation><orgName type="division">Department of Virology</orgName><orgName type="division">State Key Laboratory of Pathogens and Biosecurity</orgName><orgName type="institution">Beijing Institute of Microbiology and Epidemiology</orgName><address><settlement>Beijing</settlement><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">Qingyu</forename><surname>Zhu</surname></persName><affiliation><orgName type="division">Department of Virology</orgName><orgName type="division">State Key Laboratory of Pathogens and Biosecurity</orgName><orgName type="institution">Beijing Institute of Microbiology and Epidemiology</orgName><address><settlement>Beijing</settlement><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0008"><persName><forename type="first">Tao</forename><surname>jiang</surname></persName><affiliation><orgName type="division">Department of Virology</orgName><orgName type="division">State Key Laboratory of Pathogens and Biosecurity</orgName><orgName type="institution">Beijing Institute of Microbiology and Epidemiology</orgName><address><settlement>Beijing</settlement><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0009" role="corresp"><persName><forename type="first">Jing</forename><surname>Li</surname></persName><affiliation><orgName type="division">Department of Virology</orgName><orgName type="division">State Key Laboratory of Pathogens and Biosecurity</orgName><orgName type="institution">Beijing Institute of Microbiology and Epidemiology</orgName><address><settlement>Beijing</settlement><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0010" role="corresp"><persName><forename 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Results demonstrated that rVN‐E190G virus increased the binding avidity to α2,6 SA (sialic acid) and reduced the affinity to α2,3 SA, meanwhile weakened the viral replication in vitro. Moreover, the virulence assessment demonstrated that rVN‐E190G was attenuated in mice. These results indicated that the mutation E190G in HA decreases H5N1 viral replication in vitro and significantly attenuates virulence in vivo. These findings identify one of the determinants in RBD which can be associated with H5N1 virulence in mice. <hi rend="bold"><hi rend="italic">J. Med. Virol. 87:1816–1822, 2015</hi>.</hi> © 2015 Wiley Periodicals, Inc.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="jmv24257-kwd-0001">H5N1</term><term xml:id="jmv24257-kwd-0002">hemagglutinin</term><term xml:id="jmv24257-kwd-0003">receptor binding domain</term><term xml:id="jmv24257-kwd-0004">mouse model</term><term xml:id="jmv24257-kwd-0005">attenuation</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-8W33562B-J/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="jmv24257"><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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E‐mail: <email>lj-pbs@163.com</email> (J. L.); <email>qincf@bmi.ac.cn</email> (C. Q.)</line></lineatedText></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JMV.JMV24257.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Mouse lung‐adapted mutation of E190G in hemagglutinin from H5N1 influenza virus contributes to attenuation in mice</title><title type="short">E190G in HA of H5N1 Confer Attenuation</title><title type="shortAuthors">Han et al</title></titleGroup><creators><creator xml:id="jmv24257-cr-0001" creatorRole="author" affiliationRef="#jmv24257-aff-0001"><personName><givenNames>Pengfei</givenNames> <familyName>Han</familyName></personName></creator><creator xml:id="jmv24257-cr-0002" creatorRole="author" affiliationRef="#jmv24257-aff-0001"><personName><givenNames>Yi</givenNames> <familyName>Hu</familyName></personName></creator><creator xml:id="jmv24257-cr-0003" creatorRole="author" affiliationRef="#jmv24257-aff-0001"><personName><givenNames>Wei</givenNames> <familyName>Sun</familyName></personName></creator><creator xml:id="jmv24257-cr-0004" creatorRole="author" affiliationRef="#jmv24257-aff-0001"><personName><givenNames>Sen</givenNames> <familyName>Zhang</familyName></personName></creator><creator xml:id="jmv24257-cr-0005" creatorRole="author" affiliationRef="#jmv24257-aff-0001"><personName><givenNames>Yuchang</givenNames> <familyName>Li</familyName></personName></creator><creator xml:id="jmv24257-cr-0006" creatorRole="author" affiliationRef="#jmv24257-aff-0001"><personName><givenNames>Xiaoyan</givenNames> <familyName>Wu</familyName></personName></creator><creator xml:id="jmv24257-cr-0007" creatorRole="author" affiliationRef="#jmv24257-aff-0001"><personName><givenNames>Yinhui</givenNames> <familyName>Yang</familyName></personName></creator><creator xml:id="jmv24257-cr-0008" creatorRole="author" affiliationRef="#jmv24257-aff-0001"><personName><givenNames>Qingyu</givenNames> <familyName>Zhu</familyName></personName></creator><creator xml:id="jmv24257-cr-0009" creatorRole="author" affiliationRef="#jmv24257-aff-0001"><personName><givenNames>Tao</givenNames> <familyName>jiang</familyName></personName></creator><creator xml:id="jmv24257-cr-0010" creatorRole="author" affiliationRef="#jmv24257-aff-0001" corresponding="yes"><personName><givenNames>Jing</givenNames> <familyName>Li</familyName></personName></creator><creator xml:id="jmv24257-cr-0011" creatorRole="author" affiliationRef="#jmv24257-aff-0001" corresponding="yes"><personName><givenNames>Chengfeng</givenNames> <familyName>Qin</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="jmv24257-aff-0001" countryCode="CN"><orgDiv>Department of Virology</orgDiv><orgDiv>State Key Laboratory of Pathogens and Biosecurity</orgDiv><orgName>Beijing Institute of Microbiology and Epidemiology</orgName><address><city>Beijing</city><country>PR China</country></address></affiliation></affiliationGroup><keywordGroup type="author" xml:lang="en"><keyword xml:id="jmv24257-kwd-0001">H5N1</keyword><keyword xml:id="jmv24257-kwd-0002">hemagglutinin</keyword><keyword xml:id="jmv24257-kwd-0003">receptor binding domain</keyword><keyword xml:id="jmv24257-kwd-0004">mouse model</keyword><keyword xml:id="jmv24257-kwd-0005">attenuation</keyword></keywordGroup><fundingInfo><fundingAgency>National Nature Science Foundation of China</fundingAgency><fundingNumber>31200119</fundingNumber></fundingInfo><fundingInfo><fundingAgency>National 973 Projects</fundingAgency><fundingNumber>2011CB504706 and 2012CB518904</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><section xml:id="jmv24257-sec-0001"><p>The highly pathogenic H5N1 avian influenza virus is one of the greatest influenza pandemic threats since 2003. The association of the receptor binding domain (RBD) with the virulence of influenza virus is rarely addressed, particularly of H5N1 influenza viruses. In this study, BALB/c mice were intranasally infected with A/Vietnam/1194/2004 (VN1194, H5N1). The mouse lung‐adapted variants were isolated and the mutation of E190G (H3 numbering) in the RBD was recognized. The recombinant virus, rVN‐E190G carrying E190G in hemagglutinin (HA) was designed and rescued using reverse genetics techniques. The receptor binding activity, growth curve and pathogenicity in mice of the rVN‐E190G were investigated. Results demonstrated that rVN‐E190G virus increased the binding avidity to α2,6 SA (sialic acid) and reduced the affinity to α2,3 SA, meanwhile weakened the viral replication in vitro. Moreover, the virulence assessment demonstrated that rVN‐E190G was attenuated in mice. These results indicated that the mutation E190G in HA decreases H5N1 viral replication in vitro and significantly attenuates virulence in vivo. These findings identify one of the determinants in RBD which can be associated with H5N1 virulence in mice. <b><i>J. Med. Virol. 87:1816–1822, 2015</i>.</b> © 2015 Wiley Periodicals, Inc.</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Mouse lung‐adapted mutation of E190G in hemagglutinin from H5N1 influenza virus contributes to attenuation in mice</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>E190G in HA of H5N1 Confer Attenuation</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mouse lung‐adapted mutation of E190G in hemagglutinin from H5N1 influenza virus contributes to attenuation in mice</title></titleInfo><name type="personal"><namePart type="given">Pengfei</namePart><namePart type="family">Han</namePart><affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yi</namePart><namePart type="family">Hu</namePart><affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wei</namePart><namePart type="family">Sun</namePart><affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sen</namePart><namePart type="family">Zhang</namePart><affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yuchang</namePart><namePart type="family">Li</namePart><affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Xiaoyan</namePart><namePart type="family">Wu</namePart><affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yinhui</namePart><namePart type="family">Yang</namePart><affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Qingyu</namePart><namePart type="family">Zhu</namePart><affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tao</namePart><namePart type="family">jiang</namePart><affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jing</namePart><namePart type="family">Li</namePart><affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</affiliation><affiliation>Correspondence to: Jing Li and Chengfeng Qin, No. 20, Dongda Street, Fengtai District, Beijing 100071, PR China. E‐mail: (J. L.); (C. Q.)</affiliation><affiliation>E-mail: lj-pbs@163.comqincf@bmi.ac.cn</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chengfeng</namePart><namePart type="family">Qin</namePart><affiliation>Department of Virology, State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, PR China</affiliation><affiliation>Correspondence to: Jing Li and Chengfeng Qin, No. 20, Dongda Street, Fengtai District, Beijing 100071, PR China. E‐mail: (J. L.); (C. Q.)</affiliation><affiliation>E-mail: lj-pbs@163.comqincf@bmi.ac.cn</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">2015-11</dateIssued><dateCreated encoding="w3cdtf">2015-07-28</dateCreated><dateValid encoding="w3cdtf">2015-05-04</dateValid><copyrightDate encoding="w3cdtf">2015</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">The highly pathogenic H5N1 avian influenza virus is one of the greatest influenza pandemic threats since 2003. The association of the receptor binding domain (RBD) with the virulence of influenza virus is rarely addressed, particularly of H5N1 influenza viruses. In this study, BALB/c mice were intranasally infected with A/Vietnam/1194/2004 (VN1194, H5N1). The mouse lung‐adapted variants were isolated and the mutation of E190G (H3 numbering) in the RBD was recognized. The recombinant virus, rVN‐E190G carrying E190G in hemagglutinin (HA) was designed and rescued using reverse genetics techniques. The receptor binding activity, growth curve and pathogenicity in mice of the rVN‐E190G were investigated. Results demonstrated that rVN‐E190G virus increased the binding avidity to α2,6 SA (sialic acid) and reduced the affinity to α2,3 SA, meanwhile weakened the viral replication in vitro. Moreover, the virulence assessment demonstrated that rVN‐E190G was attenuated in mice. These results indicated that the mutation E190G in HA decreases H5N1 viral replication in vitro and significantly attenuates virulence in vivo. These findings identify one of the determinants in RBD which can be associated with H5N1 virulence in mice. J. Med. Virol. 87:1816–1822, 2015. © 2015 Wiley Periodicals, Inc.</abstract><note type="funding">National Nature Science Foundation of China - No. 31200119; </note><note type="funding">National 973 Projects - No. 2011CB504706 and 2012CB518904; </note><subject lang="en"><genre>keywords</genre><topic>H5N1</topic><topic>hemagglutinin</topic><topic>receptor binding domain</topic><topic>mouse model</topic><topic>attenuation</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Medical Virology</title></titleInfo><titleInfo type="abbreviated"><title>J. Med. Virol.</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><subject><genre>article-category</genre><topic>Research Article</topic><topic>Research Articles</topic></subject><identifier type="ISSN">0146-6615</identifier><identifier type="eISSN">1096-9071</identifier><identifier type="DOI">10.1002/(ISSN)1096-9071</identifier><identifier type="PublisherID">JMV</identifier><part><date>2015</date><detail type="volume"><caption>vol.</caption><number>87</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>1816</start><end>1822</end><total>7</total></extent></part></relatedItem><relatedItem type="references" displayLabel="jmv24257-cit-0001"><titleInfo><title>Pattern of mutation in the genome of influenza A virus on adaptation to increased virulence in the mouse lung: Identification of functional themes</title></titleInfo><name type="personal"><namePart type="given">EG</namePart><namePart type="family">Brown</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Liu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LC</namePart><namePart type="family">Kit</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Baird</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Nesrallah</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Brown EG, Liu H, Kit LC, Baird S, Nesrallah M. 2001. 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