Changes in H3 influenza A virus receptor specificity during replication in humans
Identifieur interne : 000B02 ( Istex/Corpus ); précédent : 000B01; suivant : 000B03Changes in H3 influenza A virus receptor specificity during replication in humans
Auteurs : Kathleen Ryan-Poirier ; Yasuo Suzuki ; William J. Bean ; Darwyn Kobasa ; Ayato Takada ; Toshihiro Ito ; Yoshihiro KawaokaSource :
- Virus Research [ 0168-1702 ] ; 1998.
English descriptors
- Teeft :
- Amino, Amino acid changes, Assay, Avian, Avian virus, Binding activity, Binding assay, Chain type, Chicken erythrocytes, Distinct glycoprotein inhibitors, Elsevier science, Gangliosides, Hemagglutination inhibition, Hemagglutinin, Horse serum, Host species, Human population, Human viruses, Infectious diseases, Inhibitor, Jude research hospital, Kawaoka, Linkage, Neutralization, Other viruses, Paulson, Potential glycosylation site, Present address, Rabbit sera, Receptor, Receptor binding, Receptor changes, Receptor determinants, Respiratory epithelium, Room temperature, Serum inhibitor sensitivity, Serum inhibitors, Serum sensitivity, Sialic, Sialic acid, Suzuki, Veterinary medicine, Viral infectivity, Virol, Virology, Virus, Virus binding, Virus hemagglutinin, Virus infection, Virus receptor, Virus research.
Abstract
Abstract: Influenza A viruses of the H3 subtype caused the 1968 Hong Kong pandemic, the hemagglutinin (HA) gene being introduced into humans following a reassortment event with an avian virus. Receptor specificity and serum inhibitor sensitivity of the HA of influenza A viruses are linked to the host species. Human H3 viruses preferentially recognize N-acetyl sialic acid linked to galactose by α2,6 linkages (Neu5Acα2,6Gal) and are sensitive to serum inhibitors, whereas avian and equine viruses preferentially recognize Neu5Acα2,3Gal linkages and are resistant to serum inhibitors. We have examined the receptor specificity and serum inhibitor sensitivity of H3 human influenza A viruses from the time they were introduced into the human population to gain insight into the mechanism of viral molecular evolution and host tropism. All of the viruses were sensitive to neutralization and hemagglutination inhibition by horse serum. Early H3 viruses were resistant to pig and rabbit serum inhibitors. Viruses isolated after 1977 were uniformly sensitive to inhibition by pig and rabbit sera. The recognition of Neu5Acα2,3Gal or Neu5Acα2,6Gal linkages was not correlated with the serum sensitivity. These data showed that the receptor specificity of HA, measured as inhibitor sensitivity, has changed during replication in humans since its introduction from an avian virus.
Url:
DOI: 10.1016/S0168-1702(98)00067-7
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ISTEX:87A95EBC891DB1FF395035DF4A195C20706CD65CLe document en format XML
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Bean</name><affiliation><mods:affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</mods:affiliation></affiliation></author><author><name sortKey="Kobasa, Darwyn" sort="Kobasa, Darwyn" uniqKey="Kobasa D" first="Darwyn" last="Kobasa">Darwyn Kobasa</name><affiliation><mods:affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</mods:affiliation></affiliation></author><author><name sortKey="Takada, Ayato" sort="Takada, Ayato" uniqKey="Takada A" first="Ayato" last="Takada">Ayato Takada</name><affiliation><mods:affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</mods:affiliation></affiliation></author><author><name sortKey="Ito, Toshihiro" sort="Ito, Toshihiro" uniqKey="Ito T" first="Toshihiro" last="Ito">Toshihiro Ito</name><affiliation><mods:affiliation>Department of Veterinary Public Health, Faculty of Agriculture, Tottori University, Tottori 680, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kawaoka, Yoshihiro" sort="Kawaoka, Yoshihiro" uniqKey="Kawaoka Y" first="Yoshihiro" last="Kawaoka">Yoshihiro Kawaoka</name><affiliation><mods:affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:87A95EBC891DB1FF395035DF4A195C20706CD65C</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1016/S0168-1702(98)00067-7</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-FX44HDX4-K/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000B02</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000B02</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Changes in H3 influenza A virus receptor specificity during replication in humans</title><author><name sortKey="Ryan Poirier, Kathleen" sort="Ryan Poirier, Kathleen" uniqKey="Ryan Poirier K" first="Kathleen" last="Ryan-Poirier">Kathleen Ryan-Poirier</name><affiliation><mods:affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</mods:affiliation></affiliation></author><author><name sortKey="Suzuki, Yasuo" sort="Suzuki, Yasuo" uniqKey="Suzuki Y" first="Yasuo" last="Suzuki">Yasuo Suzuki</name><affiliation><mods:affiliation>Department of Biochemistry, University of Shizuoka, School of Pharmaceutical Science, Yada, Shizuoka-Shi 422, Japan</mods:affiliation></affiliation></author><author><name sortKey="Bean, William J" sort="Bean, William J" uniqKey="Bean W" first="William J" last="Bean">William J. Bean</name><affiliation><mods:affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</mods:affiliation></affiliation></author><author><name sortKey="Kobasa, Darwyn" sort="Kobasa, Darwyn" uniqKey="Kobasa D" first="Darwyn" last="Kobasa">Darwyn Kobasa</name><affiliation><mods:affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</mods:affiliation></affiliation></author><author><name sortKey="Takada, Ayato" sort="Takada, Ayato" uniqKey="Takada A" first="Ayato" last="Takada">Ayato Takada</name><affiliation><mods:affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</mods:affiliation></affiliation></author><author><name sortKey="Ito, Toshihiro" sort="Ito, Toshihiro" uniqKey="Ito T" first="Toshihiro" last="Ito">Toshihiro Ito</name><affiliation><mods:affiliation>Department of Veterinary Public Health, Faculty of Agriculture, Tottori University, Tottori 680, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kawaoka, Yoshihiro" sort="Kawaoka, Yoshihiro" uniqKey="Kawaoka Y" first="Yoshihiro" last="Kawaoka">Yoshihiro Kawaoka</name><affiliation><mods:affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Virus Research</title><title level="j" type="abbrev">VIRUS</title><idno type="ISSN">0168-1702</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998">1998</date><biblScope unit="volume">56</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="169">169</biblScope><biblScope unit="page" to="176">176</biblScope></imprint><idno type="ISSN">0168-1702</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0168-1702</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Amino</term><term>Amino acid changes</term><term>Assay</term><term>Avian</term><term>Avian virus</term><term>Binding activity</term><term>Binding assay</term><term>Chain type</term><term>Chicken erythrocytes</term><term>Distinct glycoprotein inhibitors</term><term>Elsevier science</term><term>Gangliosides</term><term>Hemagglutination inhibition</term><term>Hemagglutinin</term><term>Horse serum</term><term>Host species</term><term>Human population</term><term>Human viruses</term><term>Infectious diseases</term><term>Inhibitor</term><term>Jude research hospital</term><term>Kawaoka</term><term>Linkage</term><term>Neutralization</term><term>Other viruses</term><term>Paulson</term><term>Potential glycosylation site</term><term>Present address</term><term>Rabbit sera</term><term>Receptor</term><term>Receptor binding</term><term>Receptor changes</term><term>Receptor determinants</term><term>Respiratory epithelium</term><term>Room temperature</term><term>Serum inhibitor sensitivity</term><term>Serum inhibitors</term><term>Serum sensitivity</term><term>Sialic</term><term>Sialic acid</term><term>Suzuki</term><term>Veterinary medicine</term><term>Viral infectivity</term><term>Virol</term><term>Virology</term><term>Virus</term><term>Virus binding</term><term>Virus hemagglutinin</term><term>Virus infection</term><term>Virus receptor</term><term>Virus research</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Influenza A viruses of the H3 subtype caused the 1968 Hong Kong pandemic, the hemagglutinin (HA) gene being introduced into humans following a reassortment event with an avian virus. Receptor specificity and serum inhibitor sensitivity of the HA of influenza A viruses are linked to the host species. Human H3 viruses preferentially recognize N-acetyl sialic acid linked to galactose by α2,6 linkages (Neu5Acα2,6Gal) and are sensitive to serum inhibitors, whereas avian and equine viruses preferentially recognize Neu5Acα2,3Gal linkages and are resistant to serum inhibitors. We have examined the receptor specificity and serum inhibitor sensitivity of H3 human influenza A viruses from the time they were introduced into the human population to gain insight into the mechanism of viral molecular evolution and host tropism. All of the viruses were sensitive to neutralization and hemagglutination inhibition by horse serum. Early H3 viruses were resistant to pig and rabbit serum inhibitors. Viruses isolated after 1977 were uniformly sensitive to inhibition by pig and rabbit sera. The recognition of Neu5Acα2,3Gal or Neu5Acα2,6Gal linkages was not correlated with the serum sensitivity. These data showed that the receptor specificity of HA, measured as inhibitor sensitivity, has changed during replication in humans since its introduction from an avian virus.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>receptor</json:string><json:string>paulson</json:string><json:string>rabbit sera</json:string><json:string>kawaoka</json:string><json:string>gangliosides</json:string><json:string>avian</json:string><json:string>sialic</json:string><json:string>virus research</json:string><json:string>virology</json:string><json:string>virol</json:string><json:string>hemagglutinin</json:string><json:string>serum inhibitor sensitivity</json:string><json:string>inhibitor</json:string><json:string>horse serum</json:string><json:string>assay</json:string><json:string>serum inhibitors</json:string><json:string>receptor binding</json:string><json:string>amino</json:string><json:string>virus</json:string><json:string>suzuki</json:string><json:string>other viruses</json:string><json:string>chain type</json:string><json:string>present address</json:string><json:string>jude research hospital</json:string><json:string>potential glycosylation site</json:string><json:string>amino acid changes</json:string><json:string>serum sensitivity</json:string><json:string>human population</json:string><json:string>room temperature</json:string><json:string>hemagglutination inhibition</json:string><json:string>linkage</json:string><json:string>neutralization</json:string><json:string>host species</json:string><json:string>viral infectivity</json:string><json:string>elsevier science</json:string><json:string>respiratory epithelium</json:string><json:string>distinct glycoprotein inhibitors</json:string><json:string>chicken erythrocytes</json:string><json:string>virus binding</json:string><json:string>sialic acid</json:string><json:string>human viruses</json:string><json:string>binding activity</json:string><json:string>binding assay</json:string><json:string>avian virus</json:string><json:string>receptor changes</json:string><json:string>veterinary medicine</json:string><json:string>infectious diseases</json:string><json:string>virus hemagglutinin</json:string><json:string>virus receptor</json:string><json:string>receptor determinants</json:string><json:string>virus infection</json:string></teeft></keywords><author><json:item><name>Kathleen Ryan-Poirier</name><affiliations><json:string>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</json:string></affiliations></json:item><json:item><name>Yasuo Suzuki</name><affiliations><json:string>Department of Biochemistry, University of Shizuoka, School of Pharmaceutical Science, Yada, Shizuoka-Shi 422, Japan</json:string></affiliations></json:item><json:item><name>William J Bean</name><affiliations><json:string>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</json:string></affiliations></json:item><json:item><name>Darwyn Kobasa</name><affiliations><json:string>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</json:string></affiliations></json:item><json:item><name>Ayato Takada</name><affiliations><json:string>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</json:string></affiliations></json:item><json:item><name>Toshihiro Ito</name><affiliations><json:string>Department of Veterinary Public Health, Faculty of Agriculture, Tottori University, Tottori 680, Japan</json:string></affiliations></json:item><json:item><name>Yoshihiro Kawaoka</name><affiliations><json:string>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Influenza virus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Receptor specificity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Serum inhibitor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Hemagglutinin</value></json:item></subject><arkIstex>ark:/67375/6H6-FX44HDX4-K</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Influenza A viruses of the H3 subtype caused the 1968 Hong Kong pandemic, the hemagglutinin (HA) gene being introduced into humans following a reassortment event with an avian virus. Receptor specificity and serum inhibitor sensitivity of the HA of influenza A viruses are linked to the host species. Human H3 viruses preferentially recognize N-acetyl sialic acid linked to galactose by α2,6 linkages (Neu5Acα2,6Gal) and are sensitive to serum inhibitors, whereas avian and equine viruses preferentially recognize Neu5Acα2,3Gal linkages and are resistant to serum inhibitors. We have examined the receptor specificity and serum inhibitor sensitivity of H3 human influenza A viruses from the time they were introduced into the human population to gain insight into the mechanism of viral molecular evolution and host tropism. All of the viruses were sensitive to neutralization and hemagglutination inhibition by horse serum. Early H3 viruses were resistant to pig and rabbit serum inhibitors. Viruses isolated after 1977 were uniformly sensitive to inhibition by pig and rabbit sera. The recognition of Neu5Acα2,3Gal or Neu5Acα2,6Gal linkages was not correlated with the serum sensitivity. These data showed that the receptor specificity of HA, measured as inhibitor sensitivity, has changed during replication in humans since its introduction from an avian virus.</abstract><qualityIndicators><score>8.175</score><pdfWordCount>3739</pdfWordCount><pdfCharCount>24969</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>8</pdfPageCount><pdfPageSize>535 x 675 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>203</abstractWordCount><abstractCharCount>1374</abstractCharCount><keywordCount>4</keywordCount></qualityIndicators><title>Changes in H3 influenza A virus receptor specificity during replication in humans</title><pmid><json:string>9783465</json:string></pmid><pii><json:string>S0168-1702(98)00067-7</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Virus Research</title><language><json:string>unknown</json:string></language><publicationDate>1998</publicationDate><issn><json:string>0168-1702</json:string></issn><pii><json:string>S0168-1702(00)X0042-1</json:string></pii><volume>56</volume><issue>2</issue><pages><first>169</first><last>176</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1968</json:string><json:string>1975</json:string><json:string>1998</json:string><json:string>1976</json:string><json:string>1972</json:string><json:string>1970s</json:string><json:string>1977</json:string><json:string>1024</json:string></date><geogName></geogName><orgName><json:string>ALSAC</json:string><json:string>Department of Pathology, Uni</json:string><json:string>Jude Children’s Research Hospital</json:string><json:string>Biologics Evaluation and Research, FDA, Bethesda, MD</json:string><json:string>American Lebanese Syrian Associated Charities</json:string><json:string>Jackson Immuno Research Laboratories, West Grove, PA</json:string><json:string>National Institute of Allergy and Infectious Diseases</json:string><json:string>Department of Veterinary Public Health, Faculty of Agriculture, Tottori Uni</json:string><json:string>Cancer Center Support</json:string><json:string>Department of Pediatrics, Uni</json:string><json:string>Medical Center, Memphis</json:string><json:string>Jude Children’s Research Hospital, Memphis, TN</json:string><json:string>Laboratory of Microbiology, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido Uni</json:string><json:string>CORE</json:string><json:string>Department of Infectious Diseases, St</json:string><json:string>Department of Biochemistry, Uni</json:string><json:string>Grant CA-21765</json:string><json:string>Public Health Service Grant AI-33898</json:string></orgName><orgName_funder><json:string>Grant CA-21765</json:string><json:string>Public Health Service Grant AI-33898</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Sue Watson</json:string><json:string>Krisna Wells</json:string><json:string>William J. Bean</json:string></persName><placeName><json:string>Kyoto</json:string><json:string>Germany</json:string><json:string>Shizuoka</json:string><json:string>Madison</json:string><json:string>Los Angeles</json:string><json:string>Japan</json:string><json:string>TN</json:string><json:string>Memphis</json:string><json:string>WI</json:string><json:string>Sapporo</json:string><json:string>Netherlands</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Ito et al., 1997</json:string><json:string>Smith et al., 1987</json:string><json:string>Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015</json:string><json:string>Baum and Paulson, 1990</json:string><json:string>Gottschalk, 1959</json:string><json:string>K. Ryan-Poirier et al.</json:string><json:string>Ito et al. (1997)</json:string><json:string>Ryan-Poirier and Kawaoka, 1993</json:string><json:string>Underwood et al., 1987</json:string><json:string>Pritchett and Paulson, 1989</json:string><json:string>Robertson et al., 1991</json:string><json:string>Verhoeyen et al., 1980</json:string><json:string>Reed and Muench (1938)</json:string><json:string>Rogers and Paulson, 1983</json:string><json:string>Suzuki et al., 1992</json:string><json:string>Yewdell et al., 1986</json:string><json:string>Suzuki et al., 1986</json:string><json:string>Bean et al., 1992</json:string><json:string>Ananthanarayan and Paniker, 1960</json:string><json:string>Wilson et al., 1981</json:string><json:string>Rogers et al., 1983b</json:string><json:string>Ryan-Poirier and Kawaoka, 1991</json:string><json:string>Scholtissek et al., 1978</json:string><json:string>Katz et al., 1987, 1990</json:string><json:string>Krizanova and Rathova, 1969</json:string><json:string>Weis et al., 1988</json:string><json:string>Al-Nakib and Tyrrell, 1992</json:string><json:string>Higa et al., 1985</json:string><json:string>Rogers et al., 1983a</json:string><json:string>Palmer et al., 1975</json:string><json:string>Deom et al., 1986</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-FX44HDX4-K</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 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Cancer Research</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Infectious Diseases</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and 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metabolique</json:string></inist></categories><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1016/S0168-1702(98)00067-7</json:string></doi><id>87A95EBC891DB1FF395035DF4A195C20706CD65C</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-FX44HDX4-K/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-FX44HDX4-K/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-FX44HDX4-K/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">Changes in H3 influenza A virus receptor specificity during replication in humans</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©1998 Elsevier Science B.V.</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>1998</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: Sensitivity of human H3 influenza A viruses to hemagglutination inhibition (HI) by horse, pig, and rabbit seraa</note><note type="content">Table 2: Differential neutralization of human H3 influenza A viruses by horse, pig, and rabbit seraa</note><note type="content">Table 3: Binding activity of human H3 influenza A viruses to various gangliosidesa</note><note type="content">Table 4: Alterations in HA associated with changes in receptor specificity or sensitivity to serum inhibition</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Changes in H3 influenza A virus receptor specificity during replication in humans</title><author xml:id="author-0000"><persName><forename type="first">Kathleen</forename><surname>Ryan-Poirier</surname></persName><note type="biography">Present address: The Kids' Health Team, 2841 N.W. 41st Street Suite B, Gainsville, FL 32606, USA.</note><affiliation>Present address: The Kids' Health Team, 2841 N.W. 41st Street Suite B, Gainsville, FL 32606, USA.</affiliation><affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Yasuo</forename><surname>Suzuki</surname></persName><affiliation>Department of Biochemistry, University of Shizuoka, School of Pharmaceutical Science, Yada, Shizuoka-Shi 422, Japan</affiliation></author><author xml:id="author-0002"><persName><forename type="first">William J</forename><surname>Bean</surname></persName><note type="biography">Present address: NIAID Scientific Review Program, Solar Building 4C-34, Bethesda, MD 20892, USA,</note><affiliation>Present address: NIAID Scientific Review Program, Solar Building 4C-34, Bethesda, MD 20892, USA,</affiliation><affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Darwyn</forename><surname>Kobasa</surname></persName><note type="biography">Present address: Center for Biologics Evaluation and Research, FDA, Bethesda, MD 20892, USA.</note><affiliation>Present address: Center for Biologics Evaluation and Research, FDA, Bethesda, MD 20892, USA.</affiliation><affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Ayato</forename><surname>Takada</surname></persName><affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Toshihiro</forename><surname>Ito</surname></persName><affiliation>Department of Veterinary Public Health, Faculty of Agriculture, Tottori University, Tottori 680, Japan</affiliation></author><author xml:id="author-0006"><persName><forename type="first">Yoshihiro</forename><surname>Kawaoka</surname></persName><note type="biography">Present address: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive West, Madison, WI 53706, USA.</note><note type="correspondence"><p>Corresponding author. Tel.: +1 608 2654925; fax: +1 608 2655622; e-mail: kawaokay@svm.vetmed.wisc.edu</p></note><affiliation>Present address: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive West, Madison, WI 53706, USA.</affiliation><affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</affiliation></author><idno type="istex">87A95EBC891DB1FF395035DF4A195C20706CD65C</idno><idno type="ark">ark:/67375/6H6-FX44HDX4-K</idno><idno type="DOI">10.1016/S0168-1702(98)00067-7</idno><idno type="PII">S0168-1702(98)00067-7</idno></analytic><monogr><title level="j">Virus Research</title><title level="j" type="abbrev">VIRUS</title><idno type="pISSN">0168-1702</idno><idno type="PII">S0168-1702(00)X0042-1</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998"></date><biblScope unit="volume">56</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="169">169</biblScope><biblScope unit="page" to="176">176</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Influenza A viruses of the H3 subtype caused the 1968 Hong Kong pandemic, the hemagglutinin (HA) gene being introduced into humans following a reassortment event with an avian virus. Receptor specificity and serum inhibitor sensitivity of the HA of influenza A viruses are linked to the host species. Human H3 viruses preferentially recognize N-acetyl sialic acid linked to galactose by α2,6 linkages (Neu5Acα2,6Gal) and are sensitive to serum inhibitors, whereas avian and equine viruses preferentially recognize Neu5Acα2,3Gal linkages and are resistant to serum inhibitors. We have examined the receptor specificity and serum inhibitor sensitivity of H3 human influenza A viruses from the time they were introduced into the human population to gain insight into the mechanism of viral molecular evolution and host tropism. All of the viruses were sensitive to neutralization and hemagglutination inhibition by horse serum. Early H3 viruses were resistant to pig and rabbit serum inhibitors. Viruses isolated after 1977 were uniformly sensitive to inhibition by pig and rabbit sera. The recognition of Neu5Acα2,3Gal or Neu5Acα2,6Gal linkages was not correlated with the serum sensitivity. These data showed that the receptor specificity of HA, measured as inhibitor sensitivity, has changed during replication in humans since its introduction from an avian virus.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Influenza virus</term></item><item><term>Receptor specificity</term></item><item><term>Serum inhibitor</term></item><item><term>Hemagglutinin</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-05-20">Modified</change><change when="1998">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-FX44HDX4-K/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>VIRUS</jid><aid>1638</aid><ce:pii>S0168-1702(98)00067-7</ce:pii><ce:doi>10.1016/S0168-1702(98)00067-7</ce:doi><ce:copyright year="1998" type="full-transfer">Elsevier Science B.V.</ce:copyright></item-info><head><ce:title>Changes in H3 influenza A virus receptor specificity during replication in humans</ce:title><ce:author-group><ce:author><ce:given-name>Kathleen</ce:given-name><ce:surname>Ryan-Poirier</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref><ce:cross-ref refid="AFF2">b</ce:cross-ref><ce:cross-ref refid="AFF3">c</ce:cross-ref><ce:cross-ref refid="AFF4">d</ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Yasuo</ce:given-name><ce:surname>Suzuki</ce:surname><ce:cross-ref refid="AFF5">e</ce:cross-ref></ce:author><ce:author><ce:given-name>William J</ce:given-name><ce:surname>Bean</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref><ce:cross-ref refid="FN2"><ce:sup>2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Darwyn</ce:given-name><ce:surname>Kobasa</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref><ce:cross-ref refid="FN3"><ce:sup>3</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Ayato</ce:given-name><ce:surname>Takada</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref><ce:cross-ref refid="AFF6">f</ce:cross-ref></ce:author><ce:author><ce:given-name>Toshihiro</ce:given-name><ce:surname>Ito</ce:surname><ce:cross-ref refid="AFF7">g</ce:cross-ref></ce:author><ce:author><ce:given-name>Yoshihiro</ce:given-name><ce:surname>Kawaoka</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref><ce:cross-ref refid="AFF8">h</ce:cross-ref><ce:cross-ref refid="CORR1">*</ce:cross-ref><ce:cross-ref refid="FN4"><ce:sup>4</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Department of Pediatrics, University of Tennessee, Memphis, TN 38163, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF4"><ce:label>d</ce:label><ce:textfn>Lebonheur Children's Medical Center, Memphis, TN, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF5"><ce:label>e</ce:label><ce:textfn>Department of Biochemistry, University of Shizuoka, School of Pharmaceutical Science, Yada, Shizuoka-Shi 422, Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF6"><ce:label>f</ce:label><ce:textfn>Laboratory of Microbiology, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060, Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF7"><ce:label>g</ce:label><ce:textfn>Department of Veterinary Public Health, Faculty of Agriculture, Tottori University, Tottori 680, Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF8"><ce:label>h</ce:label><ce:textfn>Department of Pathology, University of Tennessee, 800 N. Madison Avenue, Memphis, TN 38163, USA</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Tel.: +1 608 2654925; fax: +1 608 2655622; e-mail: kawaokay@svm.vetmed.wisc.edu</ce:text></ce:correspondence><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>Present address: The Kids' Health Team, 2841 N.W. 41st Street Suite B, Gainsville, FL 32606, USA.</ce:note-para></ce:footnote><ce:footnote id="FN2"><ce:label>2</ce:label><ce:note-para>Present address: NIAID Scientific Review Program, Solar Building 4C-34, Bethesda, MD 20892, USA,</ce:note-para></ce:footnote><ce:footnote id="FN3"><ce:label>3</ce:label><ce:note-para>Present address: Center for Biologics Evaluation and Research, FDA, Bethesda, MD 20892, USA.</ce:note-para></ce:footnote><ce:footnote id="FN4"><ce:label>4</ce:label><ce:note-para>Present address: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive West, Madison, WI 53706, USA.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="21" month="3" year="1998"></ce:date-received><ce:date-revised day="20" month="5" year="1998"></ce:date-revised><ce:date-accepted day="20" month="5" year="1998"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Influenza A viruses of the H3 subtype caused the 1968 Hong Kong pandemic, the hemagglutinin (HA) gene being introduced into humans following a reassortment event with an avian virus. Receptor specificity and serum inhibitor sensitivity of the HA of influenza A viruses are linked to the host species. Human H3 viruses preferentially recognize <ce:italic>N</ce:italic>-acetyl sialic acid linked to galactose by <ce:italic>α</ce:italic>2,6 linkages (Neu5Ac<ce:italic>α</ce:italic>2,6Gal) and are sensitive to serum inhibitors, whereas avian and equine viruses preferentially recognize Neu5Ac<ce:italic>α</ce:italic>2,3Gal linkages and are resistant to serum inhibitors. We have examined the receptor specificity and serum inhibitor sensitivity of H3 human influenza A viruses from the time they were introduced into the human population to gain insight into the mechanism of viral molecular evolution and host tropism. All of the viruses were sensitive to neutralization and hemagglutination inhibition by horse serum. Early H3 viruses were resistant to pig and rabbit serum inhibitors. Viruses isolated after 1977 were uniformly sensitive to inhibition by pig and rabbit sera. The recognition of Neu5Ac<ce:italic>α</ce:italic>2,3Gal or Neu5Ac<ce:italic>α</ce:italic>2,6Gal linkages was not correlated with the serum sensitivity. These data showed that the receptor specificity of HA, measured as inhibitor sensitivity, has changed during replication in humans since its introduction from an avian virus.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Influenza virus</ce:text></ce:keyword><ce:keyword><ce:text>Receptor specificity</ce:text></ce:keyword><ce:keyword><ce:text>Serum inhibitor</ce:text></ce:keyword><ce:keyword><ce:text>Hemagglutinin</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Changes in H3 influenza A virus receptor specificity during replication in humans</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Changes in H3 influenza A virus receptor specificity during replication in humans</title></titleInfo><name type="personal"><namePart type="given">Kathleen</namePart><namePart type="family">Ryan-Poirier</namePart><affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</affiliation><description>Present address: The Kids' Health Team, 2841 N.W. 41st Street Suite B, Gainsville, FL 32606, USA.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yasuo</namePart><namePart type="family">Suzuki</namePart><affiliation>Department of Biochemistry, University of Shizuoka, School of Pharmaceutical Science, Yada, Shizuoka-Shi 422, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">William J</namePart><namePart type="family">Bean</namePart><affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</affiliation><description>Present address: NIAID Scientific Review Program, Solar Building 4C-34, Bethesda, MD 20892, USA,</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Darwyn</namePart><namePart type="family">Kobasa</namePart><affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</affiliation><description>Present address: Center for Biologics Evaluation and Research, FDA, Bethesda, MD 20892, USA.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ayato</namePart><namePart type="family">Takada</namePart><affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Toshihiro</namePart><namePart type="family">Ito</namePart><affiliation>Department of Veterinary Public Health, Faculty of Agriculture, Tottori University, Tottori 680, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yoshihiro</namePart><namePart type="family">Kawaoka</namePart><affiliation>Department of a Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA</affiliation><description>Corresponding author. Tel.: +1 608 2654925; fax: +1 608 2655622; e-mail: kawaokay@svm.vetmed.wisc.edu</description><description>Present address: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive West, Madison, WI 53706, USA.</description><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">1998</dateIssued><dateModified encoding="w3cdtf">1998-05-20</dateModified><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Influenza A viruses of the H3 subtype caused the 1968 Hong Kong pandemic, the hemagglutinin (HA) gene being introduced into humans following a reassortment event with an avian virus. Receptor specificity and serum inhibitor sensitivity of the HA of influenza A viruses are linked to the host species. Human H3 viruses preferentially recognize N-acetyl sialic acid linked to galactose by α2,6 linkages (Neu5Acα2,6Gal) and are sensitive to serum inhibitors, whereas avian and equine viruses preferentially recognize Neu5Acα2,3Gal linkages and are resistant to serum inhibitors. We have examined the receptor specificity and serum inhibitor sensitivity of H3 human influenza A viruses from the time they were introduced into the human population to gain insight into the mechanism of viral molecular evolution and host tropism. All of the viruses were sensitive to neutralization and hemagglutination inhibition by horse serum. Early H3 viruses were resistant to pig and rabbit serum inhibitors. Viruses isolated after 1977 were uniformly sensitive to inhibition by pig and rabbit sera. The recognition of Neu5Acα2,3Gal or Neu5Acα2,6Gal linkages was not correlated with the serum sensitivity. These data showed that the receptor specificity of HA, measured as inhibitor sensitivity, has changed during replication in humans since its introduction from an avian virus.</abstract><note type="content">Table 1: Sensitivity of human H3 influenza A viruses to hemagglutination inhibition (HI) by horse, pig, and rabbit seraa</note><note type="content">Table 2: Differential neutralization of human H3 influenza A viruses by horse, pig, and rabbit seraa</note><note type="content">Table 3: Binding activity of human H3 influenza A viruses to various gangliosidesa</note><note type="content">Table 4: Alterations in HA associated with changes in receptor specificity or sensitivity to serum inhibition</note><subject><genre>Keywords</genre><topic>Influenza virus</topic><topic>Receptor specificity</topic><topic>Serum inhibitor</topic><topic>Hemagglutinin</topic></subject><relatedItem type="host"><titleInfo><title>Virus Research</title></titleInfo><titleInfo type="abbreviated"><title>VIRUS</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">1998</dateIssued></originInfo><identifier type="ISSN">0168-1702</identifier><identifier type="PII">S0168-1702(00)X0042-1</identifier><part><date>1998</date><detail type="volume"><number>56</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>125</start><end>232</end></extent><extent unit="pages"><start>169</start><end>176</end></extent></part></relatedItem><identifier type="istex">87A95EBC891DB1FF395035DF4A195C20706CD65C</identifier><identifier type="ark">ark:/67375/6H6-FX44HDX4-K</identifier><identifier type="DOI">10.1016/S0168-1702(98)00067-7</identifier><identifier type="PII">S0168-1702(98)00067-7</identifier><accessCondition type="use and reproduction" contentType="copyright">©1998 Elsevier Science B.V.</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>Elsevier Science B.V., ©1998</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-FX44HDX4-K/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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