Molecular correlates of influenza A H5N1 virus pathogenesis in mice
Identifieur interne : 000833 ( Istex/Corpus ); précédent : 000832; suivant : 000834Molecular correlates of influenza A H5N1 virus pathogenesis in mice
Auteurs : K. Subbarao ; X. Lu ; T. M Tumpey ; C. B Smith ; M. W Shaw ; J. M KatzSource :
- International congress series [ 0531-5131 ] ; 2001.
English descriptors
- Teeft :
- Acid residues, Avian influenza, Avian influenza viruses, Determinant, Embryonated hens, Gene segments, General virulence, High pathogenicity, Hong kong, Host range, Human cases, Human influenza, Influenza, Influenza apoptosis, Influenza virus, Influenza virus virulence, Influenza viruses, International congress series, Mammalian model, Mammalian species, Molecular basis, Molecular correlates, Molecular determinants, Mouse model, Mouse pathogenicity, Mouse pathogenicity phenotype, Pathogenicity, Pathogenicity phenotype, Phenotype, Respiratory disease, Respiratory illness, Respiratory tract, Sequence analysis, Specific residues, Subbarao, Virol, Virulence, Virus, Virus pathogenesis.
Abstract
Abstract: Background: In 1997, highly pathogenic avian influenza A H5N1 viruses caused 18 human cases of respiratory illness and six deaths in Hong Kong. The genes of the H5N1 viruses isolated from humans were derived from avian influenza viruses, with no evidence of reassortment with human influenza viruses. The molecular determinants of human pathogenesis were not evident. Methods: The BALB/c mouse was used as a mammalian model to evaluate the biological and molecular basis of human H5N1 virus pathogenesis. Molecular correlates of H5N1 virus pathogenicity for mice were sought by analyzing the nucleotide sequence of human H5N1 viruses. Results: Based on high and low lethality for mice, the pathogenicity phenotype of 15 human H5N1 viruses was characterized; nine viruses displayed a high, five a low, and one an intermediate pathogenicity phenotype. H5N1 viruses with a high pathogenicity phenotype replicated in multiple solid organs and caused depletion of peripheral blood leukocytes. Sequence analysis determined that five specific amino acids in four proteins correlated with pathogenicity in mice. Conclusions: Alone or in combination, these specific residues are the likely determinants of virulence of human H5N1 influenza viruses in this mammalian model.
Url:
DOI: 10.1016/S0531-5131(01)00635-5
Links to Exploration step
ISTEX:AC30AE8096A1BD72234AF3B976C1FD6FD610A396Le document en format XML
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Lu</name><affiliation><mods:affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</mods:affiliation></affiliation></author><author><name sortKey="Tumpey, T M" sort="Tumpey, T M" uniqKey="Tumpey T" first="T. M" last="Tumpey">T. M Tumpey</name><affiliation><mods:affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</mods:affiliation></affiliation></author><author><name sortKey="Smith, C B" sort="Smith, C B" uniqKey="Smith C" first="C. B" last="Smith">C. 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Subbarao</name><affiliation><mods:affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: KSubbarao@cdc.gov</mods:affiliation></affiliation></author><author><name sortKey="Lu, X" sort="Lu, X" uniqKey="Lu X" first="X" last="Lu">X. Lu</name><affiliation><mods:affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</mods:affiliation></affiliation></author><author><name sortKey="Tumpey, T M" sort="Tumpey, T M" uniqKey="Tumpey T" first="T. M" last="Tumpey">T. M Tumpey</name><affiliation><mods:affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</mods:affiliation></affiliation></author><author><name sortKey="Smith, C B" sort="Smith, C B" uniqKey="Smith C" first="C. B" last="Smith">C. B Smith</name><affiliation><mods:affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</mods:affiliation></affiliation></author><author><name sortKey="Shaw, M W" sort="Shaw, M W" uniqKey="Shaw M" first="M. W" last="Shaw">M. W Shaw</name><affiliation><mods:affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</mods:affiliation></affiliation></author><author><name sortKey="Katz, J M" sort="Katz, J M" uniqKey="Katz J" first="J. M" last="Katz">J. M Katz</name><affiliation><mods:affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">International congress series</title><title level="j" type="abbrev">ICS</title><idno type="ISSN">0531-5131</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001">2001</date><biblScope unit="volume">1219</biblScope><biblScope unit="supplement">C</biblScope><biblScope unit="page" from="595">595</biblScope><biblScope unit="page" to="600">600</biblScope></imprint><idno type="ISSN">0531-5131</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0531-5131</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acid residues</term><term>Avian influenza</term><term>Avian influenza viruses</term><term>Determinant</term><term>Embryonated hens</term><term>Gene segments</term><term>General virulence</term><term>High pathogenicity</term><term>Hong kong</term><term>Host range</term><term>Human cases</term><term>Human influenza</term><term>Influenza</term><term>Influenza apoptosis</term><term>Influenza virus</term><term>Influenza virus virulence</term><term>Influenza viruses</term><term>International congress series</term><term>Mammalian model</term><term>Mammalian species</term><term>Molecular basis</term><term>Molecular correlates</term><term>Molecular determinants</term><term>Mouse model</term><term>Mouse pathogenicity</term><term>Mouse pathogenicity phenotype</term><term>Pathogenicity</term><term>Pathogenicity phenotype</term><term>Phenotype</term><term>Respiratory disease</term><term>Respiratory illness</term><term>Respiratory tract</term><term>Sequence analysis</term><term>Specific residues</term><term>Subbarao</term><term>Virol</term><term>Virulence</term><term>Virus</term><term>Virus pathogenesis</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Background: In 1997, highly pathogenic avian influenza A H5N1 viruses caused 18 human cases of respiratory illness and six deaths in Hong Kong. The genes of the H5N1 viruses isolated from humans were derived from avian influenza viruses, with no evidence of reassortment with human influenza viruses. The molecular determinants of human pathogenesis were not evident. Methods: The BALB/c mouse was used as a mammalian model to evaluate the biological and molecular basis of human H5N1 virus pathogenesis. Molecular correlates of H5N1 virus pathogenicity for mice were sought by analyzing the nucleotide sequence of human H5N1 viruses. Results: Based on high and low lethality for mice, the pathogenicity phenotype of 15 human H5N1 viruses was characterized; nine viruses displayed a high, five a low, and one an intermediate pathogenicity phenotype. H5N1 viruses with a high pathogenicity phenotype replicated in multiple solid organs and caused depletion of peripheral blood leukocytes. Sequence analysis determined that five specific amino acids in four proteins correlated with pathogenicity in mice. 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The genes of the H5N1 viruses isolated from humans were derived from avian influenza viruses, with no evidence of reassortment with human influenza viruses. The molecular determinants of human pathogenesis were not evident. Methods: The BALB/c mouse was used as a mammalian model to evaluate the biological and molecular basis of human H5N1 virus pathogenesis. Molecular correlates of H5N1 virus pathogenicity for mice were sought by analyzing the nucleotide sequence of human H5N1 viruses. Results: Based on high and low lethality for mice, the pathogenicity phenotype of 15 human H5N1 viruses was characterized; nine viruses displayed a high, five a low, and one an intermediate pathogenicity phenotype. H5N1 viruses with a high pathogenicity phenotype replicated in multiple solid organs and caused depletion of peripheral blood leukocytes. Sequence analysis determined that five specific amino acids in four proteins correlated with pathogenicity in mice. Conclusions: Alone or in combination, these specific residues are the likely determinants of virulence of human H5N1 influenza viruses in this mammalian model.</abstract><qualityIndicators><score>6.599</score><pdfWordCount>2331</pdfWordCount><pdfCharCount>14013</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>6</pdfPageCount><pdfPageSize>544 x 743 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>189</abstractWordCount><abstractCharCount>1273</abstractCharCount><keywordCount>3</keywordCount></qualityIndicators><title>Molecular correlates of influenza A H5N1 virus pathogenesis in mice</title><pii><json:string>S0531-5131(01)00635-5</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>International congress series</title><language><json:string>unknown</json:string></language><publicationDate>2001</publicationDate><issn><json:string>0531-5131</json:string></issn><pii><json:string>S0531-5131(00)X0003-9</json:string></pii><volume>1219</volume><pages><first>595</first><last>600</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1997</json:string><json:string>2001</json:string></date><geogName></geogName><orgName><json:string>International Congress Series</json:string><json:string>Hong Kong Department of Health</json:string><json:string>Division of Viral</json:string><json:string>Southeast Poultry Research Laboratories, Athens, GA, USA</json:string><json:string>Charles River Laboratories, Wilmington</json:string><json:string>National Center for Infectious Diseases, Centers for Disease Control and Prevention</json:string><json:string>Epidemiology Section of the Influenza Branch</json:string><json:string>CDC</json:string></orgName><orgName_funder><json:string>Epidemiology Section of the Influenza Branch</json:string><json:string>CDC</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Studies</json:string><json:string>Paul Saw</json:string><json:string>Hong Kong</json:string><json:string>C.B. Smith</json:string><json:string>Sarah Cantrell</json:string><json:string>B.V. Keywords</json:string><json:string>X. Lu</json:string><json:string>K.H. Mak</json:string><json:string>Alexander Klimov</json:string><json:string>K. Subbarao</json:string><json:string>Mark Hemphill</json:string><json:string>T.M. Tumpey</json:string><json:string>M.W. Shaw</json:string></persName><placeName><json:string>Hong Kong</json:string><json:string>GA</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>[9,23]</json:string><json:string>[21,22]</json:string><json:string>[18]</json:string><json:string>[11]</json:string><json:string>[9,11]</json:string><json:string>[8]</json:string><json:string>[8,14]</json:string><json:string>K. Subbarao et al.</json:string><json:string>[5,6,8,9,12]</json:string><json:string>[15]</json:string><json:string>[19,20]</json:string><json:string>[13]</json:string><json:string>[16,17]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-T80WJBCF-1</json:string></ark><categories><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string><json:string>4 - pathologie infectieuse</json:string></inist></categories><publicationDate>2001</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1016/S0531-5131(01)00635-5</json:string></doi><id>AC30AE8096A1BD72234AF3B976C1FD6FD610A396</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-T80WJBCF-1/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-T80WJBCF-1/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-T80WJBCF-1/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">Molecular correlates of influenza A H5N1 virus pathogenesis in mice</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>elsevier</p></licence></availability><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p><date>2001</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">Table 1: Nucleotide and deduced amino acid residues in the NA, M1, PB1, and PB2 proteins that correlate with mouse pathogenicity phenotype</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Molecular correlates of influenza A H5N1 virus pathogenesis in mice</title><author xml:id="author-0000"><persName><forename type="first">K</forename><surname>Subbarao</surname></persName><email>KSubbarao@cdc.gov</email><note type="correspondence"><p>Corresponding author. Tel.: +1-404-639-3591; fax: +1-404-639-2334</p></note><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</affiliation></author><author xml:id="author-0001"><persName><forename type="first">X</forename><surname>Lu</surname></persName><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</affiliation></author><author xml:id="author-0002"><persName><forename type="first">T.M</forename><surname>Tumpey</surname></persName><note type="biography">Present address: USDA/ARS/Southeast Poultry Research Laboratories, Athens, GA, USA.</note><affiliation>Present address: USDA/ARS/Southeast Poultry Research Laboratories, Athens, GA, USA.</affiliation><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</affiliation></author><author xml:id="author-0003"><persName><forename type="first">C.B</forename><surname>Smith</surname></persName><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</affiliation></author><author xml:id="author-0004"><persName><forename type="first">M.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, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</affiliation></author><author xml:id="author-0005"><persName><forename type="first">J.M</forename><surname>Katz</surname></persName><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</affiliation></author><idno type="istex">AC30AE8096A1BD72234AF3B976C1FD6FD610A396</idno><idno type="ark">ark:/67375/6H6-T80WJBCF-1</idno><idno type="DOI">10.1016/S0531-5131(01)00635-5</idno><idno type="PII">S0531-5131(01)00635-5</idno></analytic><monogr><title level="j">International congress series</title><title level="j" type="abbrev">ICS</title><idno type="pISSN">0531-5131</idno><idno type="PII">S0531-5131(00)X0003-9</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001"></date><biblScope unit="volume">1219</biblScope><biblScope unit="supplement">C</biblScope><biblScope unit="page" from="595">595</biblScope><biblScope unit="page" to="600">600</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Background: In 1997, highly pathogenic avian influenza A H5N1 viruses caused 18 human cases of respiratory illness and six deaths in Hong Kong. The genes of the H5N1 viruses isolated from humans were derived from avian influenza viruses, with no evidence of reassortment with human influenza viruses. The molecular determinants of human pathogenesis were not evident. Methods: The BALB/c mouse was used as a mammalian model to evaluate the biological and molecular basis of human H5N1 virus pathogenesis. Molecular correlates of H5N1 virus pathogenicity for mice were sought by analyzing the nucleotide sequence of human H5N1 viruses. Results: Based on high and low lethality for mice, the pathogenicity phenotype of 15 human H5N1 viruses was characterized; nine viruses displayed a high, five a low, and one an intermediate pathogenicity phenotype. H5N1 viruses with a high pathogenicity phenotype replicated in multiple solid organs and caused depletion of peripheral blood leukocytes. Sequence analysis determined that five specific amino acids in four proteins correlated with pathogenicity in mice. Conclusions: Alone or in combination, these specific residues are the likely determinants of virulence of human H5N1 influenza viruses in this mammalian model.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Molecular pathogenesis</term></item><item><term>Influenza H5N1</term></item><item><term>Mouse pathogenicity</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001">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-T80WJBCF-1/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><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"><item-info><jid>ICS</jid><aid>337</aid><ce:pii>S0531-5131(01)00635-5</ce:pii><ce:doi>10.1016/S0531-5131(01)00635-5</ce:doi><ce:copyright type="us-gov" year="2001"></ce:copyright></item-info><head><ce:title>Molecular correlates of influenza A H5N1 virus pathogenesis in mice</ce:title><ce:author-group><ce:author><ce:given-name>K</ce:given-name><ce:surname>Subbarao</ce:surname><ce:cross-ref refid="COR1">*</ce:cross-ref><ce:e-address>KSubbarao@cdc.gov</ce:e-address></ce:author><ce:author><ce:given-name>X</ce:given-name><ce:surname>Lu</ce:surname></ce:author><ce:author><ce:given-name>T.M</ce:given-name><ce:surname>Tumpey</ce:surname><ce:cross-ref refid="FN1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>C.B</ce:given-name><ce:surname>Smith</ce:surname></ce:author><ce:author><ce:given-name>M.W</ce:given-name><ce:surname>Shaw</ce:surname></ce:author><ce:author><ce:given-name>J.M</ce:given-name><ce:surname>Katz</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, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>*</ce:label><ce:text>Corresponding author. Tel.: +1-404-639-3591; fax: +1-404-639-2334</ce:text></ce:correspondence><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>Present address: USDA/ARS/Southeast Poultry Research Laboratories, Athens, GA, USA.</ce:note-para></ce:footnote></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para><ce:italic>Background</ce:italic>: In 1997, highly pathogenic avian influenza A H5N1 viruses caused 18 human cases of respiratory illness and six deaths in Hong Kong. The genes of the H5N1 viruses isolated from humans were derived from avian influenza viruses, with no evidence of reassortment with human influenza viruses. The molecular determinants of human pathogenesis were not evident. <ce:italic>Methods</ce:italic>: The BALB/c mouse was used as a mammalian model to evaluate the biological and molecular basis of human H5N1 virus pathogenesis. Molecular correlates of H5N1 virus pathogenicity for mice were sought by analyzing the nucleotide sequence of human H5N1 viruses. <ce:italic>Results</ce:italic>: Based on high and low lethality for mice, the pathogenicity phenotype of 15 human H5N1 viruses was characterized; nine viruses displayed a high, five a low, and one an intermediate pathogenicity phenotype. H5N1 viruses with a high pathogenicity phenotype replicated in multiple solid organs and caused depletion of peripheral blood leukocytes. Sequence analysis determined that five specific amino acids in four proteins correlated with pathogenicity in mice. <ce:italic>Conclusions</ce:italic>: Alone or in combination, these specific residues are the likely determinants of virulence of human H5N1 influenza viruses in this mammalian model.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Molecular pathogenesis</ce:text></ce:keyword><ce:keyword><ce:text>Influenza H5N1</ce:text></ce:keyword><ce:keyword><ce:text>Mouse pathogenicity</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Molecular correlates of influenza A H5N1 virus pathogenesis in mice</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Molecular correlates of influenza A H5N1 virus pathogenesis in mice</title></titleInfo><name type="personal"><namePart type="given">K</namePart><namePart type="family">Subbarao</namePart><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</affiliation><affiliation>E-mail: KSubbarao@cdc.gov</affiliation><description>Corresponding author. Tel.: +1-404-639-3591; fax: +1-404-639-2334</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">X</namePart><namePart type="family">Lu</namePart><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.M</namePart><namePart type="family">Tumpey</namePart><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</affiliation><description>Present address: USDA/ARS/Southeast Poultry Research Laboratories, Athens, GA, USA.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.B</namePart><namePart type="family">Smith</namePart><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.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, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.M</namePart><namePart type="family">Katz</namePart><affiliation>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333, USA</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">2001</dateIssued><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Background: In 1997, highly pathogenic avian influenza A H5N1 viruses caused 18 human cases of respiratory illness and six deaths in Hong Kong. The genes of the H5N1 viruses isolated from humans were derived from avian influenza viruses, with no evidence of reassortment with human influenza viruses. The molecular determinants of human pathogenesis were not evident. Methods: The BALB/c mouse was used as a mammalian model to evaluate the biological and molecular basis of human H5N1 virus pathogenesis. Molecular correlates of H5N1 virus pathogenicity for mice were sought by analyzing the nucleotide sequence of human H5N1 viruses. Results: Based on high and low lethality for mice, the pathogenicity phenotype of 15 human H5N1 viruses was characterized; nine viruses displayed a high, five a low, and one an intermediate pathogenicity phenotype. H5N1 viruses with a high pathogenicity phenotype replicated in multiple solid organs and caused depletion of peripheral blood leukocytes. Sequence analysis determined that five specific amino acids in four proteins correlated with pathogenicity in mice. Conclusions: Alone or in combination, these specific residues are the likely determinants of virulence of human H5N1 influenza viruses in this mammalian model.</abstract><note type="content">Table 1: Nucleotide and deduced amino acid residues in the NA, M1, PB1, and PB2 proteins that correlate with mouse pathogenicity phenotype</note><subject><genre>Keywords</genre><topic>Molecular pathogenesis</topic><topic>Influenza H5N1</topic><topic>Mouse pathogenicity</topic></subject><relatedItem type="host"><titleInfo><title>International congress series</title></titleInfo><titleInfo type="abbreviated"><title>ICS</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">2001</dateIssued></originInfo><identifier type="ISSN">0531-5131</identifier><identifier type="PII">S0531-5131(00)X0003-9</identifier><part><date>2001</date><detail type="volume"><number>1219</number><caption>vol.</caption></detail><detail type="supplement"><number>C</number><caption>Suppl.</caption></detail><extent unit="issue-pages"><start>1</start><end>1048</end></extent><extent unit="pages"><start>595</start><end>600</end></extent></part></relatedItem><identifier type="istex">AC30AE8096A1BD72234AF3B976C1FD6FD610A396</identifier><identifier type="ark">ark:/67375/6H6-T80WJBCF-1</identifier><identifier type="DOI">10.1016/S0531-5131(01)00635-5</identifier><identifier type="PII">S0531-5131(01)00635-5</identifier><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></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-T80WJBCF-1/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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