Mutations at the cleavage site of the hemagglutinin alter the pathogenicity of influenza virus a/chick/penn/83 (H5N2)
Identifieur interne : 000C12 ( Istex/Corpus ); précédent : 000C11; suivant : 000C13Mutations at the cleavage site of the hemagglutinin alter the pathogenicity of influenza virus a/chick/penn/83 (H5N2)
Auteurs : Masanobu Ohuchi ; Michaela Orlich ; Reiko Ohuchi ; Barry E. J. Simpson ; Wolfgang Garten ; Hans-Dieter Klenk ; Rudolf RottSource :
- Virology [ 0042-6822 ] ; 1989.
English descriptors
- Teeft :
- Amino, Amino acids, Apathogenic, Arginine, Asparagine, Chick embryo cells, Cleavability, Cleavage, Cleavage site, Glycoprotein, Hemagglutinin, Hemagglutinins, Host range, Influenza, Influenza virus, Influenza virus hemagglutinin, Influenza virus pathogenicity, Influenza viruses, Kawaoka, Klenk, Lysine, Mdck cells, Monoclonal antibodies, Mutation, Nucleotide, Nucleotide sequence, Oligosaccharide, Pathogenic, Pathogenicity, Plaque, Plaque variants, Point mutation, Proline, Protease, Proteolytic cleavage, Rott, Sendai virus, Trypsin, Ubiquitous proteases, Variant, Virology, Virus.
Abstract
Abstract: Six variants that form plaques in chick embryo cells in the absence of trypsin have been isolated from the apathogenic avian influenza virus A/chick/Pennsylvania/l/83 (H5N2). Unlike the wild-type, the plaque variants contain a hemagglutinin that is cleaved in chick embryo cells and MDCK cells. The variants differ also from the wild-type in their pathogenicity for chickens. Nucleotide sequence and oligosaccharide analysis of the hemagglutinin have revealed that, unlike natural isolates with increased pathogenicity (Y. Kawaoka et al., 1984, Virology 139, 303–316; Y. Kawaoka and R. G. Webster, 1985, Virology 146, 130–137), the variants obtained in vitro have retained an oligosaccharide at asparagine 11 that is believed to interfere with the cleavage site of the wild-type. However, all variants showed mutations in the hemagglutinin resulting in an increased number of basic groups at the cleavage site. These observations demonstrate that masking of the cleavage site by an oligosaccharide is overcome by an enhancement of the basic charge at the cleavage site.
Url:
DOI: 10.1016/0042-6822(89)90267-5
Links to Exploration step
ISTEX:588DD3BADFB27DFD4EC344511B9445C2909310CBLe document en format XML
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Simpson</name><affiliation><mods:affiliation>Institut für Virologie, Justus Liebig Universität, Giessen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Garten, Wolfgang" sort="Garten, Wolfgang" uniqKey="Garten W" first="Wolfgang" last="Garten">Wolfgang Garten</name><affiliation><mods:affiliation>Institut für Virologie, Philipps Universität, Marburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Klenk, Hans Dieter" sort="Klenk, Hans Dieter" uniqKey="Klenk H" first="Hans-Dieter" last="Klenk">Hans-Dieter Klenk</name><affiliation><mods:affiliation>To whom requests for reprints should be addressed.</mods:affiliation></affiliation><affiliation><mods:affiliation>Institut für Virologie, Philipps Universität, Marburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Rott, Rudolf" sort="Rott, Rudolf" uniqKey="Rott R" first="Rudolf" last="Rott">Rudolf Rott</name><affiliation><mods:affiliation>Institut für Virologie, Justus Liebig Universität, Giessen, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="ISSN">0042-6822</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1989">1989</date><biblScope unit="volume">168</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="274">274</biblScope><biblScope unit="page" to="280">280</biblScope></imprint><idno type="ISSN">0042-6822</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0042-6822</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Amino</term><term>Amino acids</term><term>Apathogenic</term><term>Arginine</term><term>Asparagine</term><term>Chick embryo cells</term><term>Cleavability</term><term>Cleavage</term><term>Cleavage site</term><term>Glycoprotein</term><term>Hemagglutinin</term><term>Hemagglutinins</term><term>Host range</term><term>Influenza</term><term>Influenza virus</term><term>Influenza virus hemagglutinin</term><term>Influenza virus pathogenicity</term><term>Influenza viruses</term><term>Kawaoka</term><term>Klenk</term><term>Lysine</term><term>Mdck cells</term><term>Monoclonal antibodies</term><term>Mutation</term><term>Nucleotide</term><term>Nucleotide sequence</term><term>Oligosaccharide</term><term>Pathogenic</term><term>Pathogenicity</term><term>Plaque</term><term>Plaque variants</term><term>Point mutation</term><term>Proline</term><term>Protease</term><term>Proteolytic cleavage</term><term>Rott</term><term>Sendai virus</term><term>Trypsin</term><term>Ubiquitous proteases</term><term>Variant</term><term>Virology</term><term>Virus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Six variants that form plaques in chick embryo cells in the absence of trypsin have been isolated from the apathogenic avian influenza virus A/chick/Pennsylvania/l/83 (H5N2). 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Simpson</name><affiliations><json:string>Institut für Virologie, Justus Liebig Universität, Giessen, Germany</json:string></affiliations></json:item><json:item><name>Wolfgang Garten</name><affiliations><json:string>Institut für Virologie, Philipps Universität, Marburg, Germany</json:string></affiliations></json:item><json:item><name>Hans-Dieter Klenk</name><affiliations><json:string>To whom requests for reprints should be addressed.</json:string><json:string>Institut für Virologie, Philipps Universität, Marburg, Germany</json:string></affiliations></json:item><json:item><name>Rudolf Rott</name><affiliations><json:string>Institut für Virologie, Justus Liebig Universität, Giessen, Germany</json:string></affiliations></json:item></author><arkIstex>ark:/67375/6H6-8H1FW8ZG-D</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Six variants that form plaques in chick embryo cells in the absence of trypsin have been isolated from the apathogenic avian influenza virus A/chick/Pennsylvania/l/83 (H5N2). Unlike the wild-type, the plaque variants contain a hemagglutinin that is cleaved in chick embryo cells and MDCK cells. The variants differ also from the wild-type in their pathogenicity for chickens. Nucleotide sequence and oligosaccharide analysis of the hemagglutinin have revealed that, unlike natural isolates with increased pathogenicity (Y. Kawaoka et al., 1984, Virology 139, 303–316; Y. Kawaoka and R. G. Webster, 1985, Virology 146, 130–137), the variants obtained in vitro have retained an oligosaccharide at asparagine 11 that is believed to interfere with the cleavage site of the wild-type. However, all variants showed mutations in the hemagglutinin resulting in an increased number of basic groups at the cleavage site. These observations demonstrate that masking of the cleavage site by an oligosaccharide is overcome by an enhancement of the basic charge at the cleavage site.</abstract><qualityIndicators><score>7.332</score><pdfWordCount>3400</pdfWordCount><pdfCharCount>25027</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>161</abstractWordCount><abstractCharCount>1079</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Mutations at the cleavage site of the hemagglutinin alter the pathogenicity of influenza virus a/chick/penn/83 (H5N2)</title><pmid><json:string>2916326</json:string></pmid><pii><json:string>0042-6822(89)90267-5</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc. Natl. Acad. Sci. USA</title><language><json:string>unknown</json:string></language><volume>84</volume><pages><first>36</first><last>40</last></pages></serie><host><title>Virology</title><language><json:string>unknown</json:string></language><publicationDate>1989</publicationDate><issn><json:string>0042-6822</json:string></issn><pii><json:string>S0042-6822(00)X0336-4</json:string></pii><volume>168</volume><issue>2</issue><pages><first>274</first><last>280</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>35S</json:string><json:string>1983</json:string><json:string>1989</json:string></date><geogName></geogName><orgName><json:string>SFB</json:string><json:string>Deutsche Forschungsgemeinschaft</json:string></orgName><orgName_funder><json:string>SFB</json:string><json:string>Deutsche Forschungsgemeinschaft</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Beate Siegmann</json:string><json:string>Webster</json:string><json:string>R. G. Webster</json:string><json:string>Kawaoka</json:string><json:string>H. Figure</json:string><json:string>Y. Kawaoka</json:string></persName><placeName><json:string>Marburg</json:string><json:string>Germany</json:string><json:string>Pathogenicity</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Kawaoka and Webster, 1985</json:string><json:string>Klenk and Rott, 1988</json:string><json:string>Klenk and Schwarz, 1987</json:string><json:string>Bosch et al., 1979</json:string><json:string>Klenk et al., 1975</json:string><json:string>Deshpande et al., 1987</json:string><json:string>Rott et al., 1984</json:string><json:string>Maxam and Gilbert, 1977</json:string><json:string>Tashiro et al., 1988</json:string><json:string>Kawaoka and Webster, 1988</json:string><json:string>Freed and Risser, 1987</json:string><json:string>Klenk and Rott, 1980</json:string><json:string>Y. Kawaoka et al., 1984</json:string><json:string>Kawaoka et al. (1984)</json:string><json:string>Schwartz, 1986</json:string><json:string>Maniatis et al., 1982</json:string><json:string>Garten et al., 1981</json:string><json:string>Air, 1979</json:string><json:string>Kawaoka eT al., 1984</json:string><json:string>Kawaoka et al., 1984</json:string><json:string>for references see Klenk and Rott, 1988</json:string><json:string>Rott and Klenk, 1986</json:string><json:string>Bosch et al., 1981</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-8H1FW8ZG-D</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - virology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - virology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Virology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences biologiques fondamentales et appliquees. psychologie</json:string></inist></categories><publicationDate>1989</publicationDate><copyrightDate>1989</copyrightDate><doi><json:string>10.1016/0042-6822(89)90267-5</json:string></doi><id>588DD3BADFB27DFD4EC344511B9445C2909310CB</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-8H1FW8ZG-D/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-8H1FW8ZG-D/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-8H1FW8ZG-D/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">Mutations at the cleavage site of the hemagglutinin alter the pathogenicity of influenza virus a/chick/penn/83 (H5N2)</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>1989</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>Sequence data from this article have been deposited with the EMBUGenBank Data Libraries under Accession No. J04325.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Mutations at the cleavage site of the hemagglutinin alter the pathogenicity of influenza virus a/chick/penn/83 (H5N2)</title><author xml:id="author-0000"><persName><forename type="first">Masanobu</forename><surname>Ohuchi</surname></persName><affiliation>Institut für Virologie, Philipps Universität, Marburg, Germany</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Michaela</forename><surname>Orlich</surname></persName><affiliation>Institut für Virologie, Justus Liebig Universität, Giessen, Germany</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Reiko</forename><surname>Ohuchi</surname></persName><affiliation>Institut für Virologie, Philipps Universität, Marburg, Germany</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Barry E.J.</forename><surname>Simpson</surname></persName><affiliation>Institut für Virologie, Justus Liebig Universität, Giessen, Germany</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Wolfgang</forename><surname>Garten</surname></persName><affiliation>Institut für Virologie, Philipps Universität, Marburg, Germany</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Hans-Dieter</forename><surname>Klenk</surname></persName><affiliation>To whom requests for reprints should be addressed.</affiliation><affiliation>Institut für Virologie, Philipps Universität, Marburg, Germany</affiliation></author><author xml:id="author-0006"><persName><forename type="first">Rudolf</forename><surname>Rott</surname></persName><affiliation>Institut für Virologie, Justus Liebig Universität, Giessen, Germany</affiliation></author><idno type="istex">588DD3BADFB27DFD4EC344511B9445C2909310CB</idno><idno type="ark">ark:/67375/6H6-8H1FW8ZG-D</idno><idno type="DOI">10.1016/0042-6822(89)90267-5</idno><idno type="PII">0042-6822(89)90267-5</idno></analytic><monogr><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="pISSN">0042-6822</idno><idno type="PII">S0042-6822(00)X0336-4</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1989"></date><biblScope unit="volume">168</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="274">274</biblScope><biblScope unit="page" to="280">280</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1989</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Six variants that form plaques in chick embryo cells in the absence of trypsin have been isolated from the apathogenic avian influenza virus A/chick/Pennsylvania/l/83 (H5N2). Unlike the wild-type, the plaque variants contain a hemagglutinin that is cleaved in chick embryo cells and MDCK cells. The variants differ also from the wild-type in their pathogenicity for chickens. Nucleotide sequence and oligosaccharide analysis of the hemagglutinin have revealed that, unlike natural isolates with increased pathogenicity (Y. Kawaoka et al., 1984, Virology 139, 303–316; Y. Kawaoka and R. G. Webster, 1985, Virology 146, 130–137), the variants obtained in vitro have retained an oligosaccharide at asparagine 11 that is believed to interfere with the cleavage site of the wild-type. However, all variants showed mutations in the hemagglutinin resulting in an increased number of basic groups at the cleavage site. These observations demonstrate that masking of the cleavage site by an oligosaccharide is overcome by an enhancement of the basic charge at the cleavage site.</p></abstract></profileDesc><revisionDesc><change when="1989">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-8H1FW8ZG-D/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: 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>YVIRO</jid><aid>89902675</aid><ce:pii>0042-6822(89)90267-5</ce:pii><ce:doi>10.1016/0042-6822(89)90267-5</ce:doi><ce:copyright type="unknown" year="1989"></ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>Sequence data from this article have been deposited with the EMBUGenBank Data Libraries under Accession No. J04325.</ce:note-para></ce:article-footnote><ce:title>Mutations at the cleavage site of the hemagglutinin alter the pathogenicity of influenza virus a/chick/penn/83 (H5N2)</ce:title><ce:author-group><ce:author><ce:given-name>Masanobu</ce:given-name><ce:surname>Ohuchi</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Michaela</ce:given-name><ce:surname>Orlich</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Reiko</ce:given-name><ce:surname>Ohuchi</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Barry E.J.</ce:given-name><ce:surname>Simpson</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Wolfgang</ce:given-name><ce:surname>Garten</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Hans-Dieter</ce:given-name><ce:surname>Klenk</ce:surname><ce:cross-ref refid="COR1"><ce:sup>2</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Rudolf</ce:given-name><ce:surname>Rott</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>∗</ce:label><ce:textfn>Institut für Virologie, Philipps Universität, Marburg, Germany</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>†</ce:label><ce:textfn>Institut für Virologie, Justus Liebig Universität, Giessen, Germany</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>2</ce:label><ce:text>To whom requests for reprints should be addressed.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="26" month="7" year="1988"></ce:date-received><ce:date-accepted day="28" month="9" year="1988"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Six variants that form plaques in chick embryo cells in the absence of trypsin have been isolated from the apathogenic avian influenza virus A/chick/Pennsylvania/l/83 (H5N2). Unlike the wild-type, the plaque variants contain a hemagglutinin that is cleaved in chick embryo cells and MDCK cells. The variants differ also from the wild-type in their pathogenicity for chickens. Nucleotide sequence and oligosaccharide analysis of the hemagglutinin have revealed that, unlike natural isolates with increased pathogenicity (<ce:cross-ref refid="BIB9">Y. Kawaoka et al., 1984, <ce:italic>Virology</ce:italic> 139, 303–316</ce:cross-ref>; <ce:cross-ref refid="BIB10">Y. Kawaoka and R. G. Webster, 1985, <ce:italic>Virology</ce:italic> 146, 130–137</ce:cross-ref>), the variants obtained <ce:italic>in vitro</ce:italic> have retained an oligosaccharide at asparagine 11 that is believed to interfere with the cleavage site of the wild-type. However, all variants showed mutations in the hemagglutinin resulting in an increased number of basic groups at the cleavage site. These observations demonstrate that masking of the cleavage site by an oligosaccharide is overcome by an enhancement of the basic charge at the cleavage site.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Mutations at the cleavage site of the hemagglutinin alter the pathogenicity of influenza virus a/chick/penn/83 (H5N2)</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Mutations at the cleavage site of the hemagglutinin alter the pathogenicity of influenza virus a/chick/penn/83 (H5N2)</title></titleInfo><name type="personal"><namePart type="given">Masanobu</namePart><namePart type="family">Ohuchi</namePart><affiliation>Institut für Virologie, Philipps Universität, Marburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michaela</namePart><namePart type="family">Orlich</namePart><affiliation>Institut für Virologie, Justus Liebig Universität, Giessen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Reiko</namePart><namePart type="family">Ohuchi</namePart><affiliation>Institut für Virologie, Philipps Universität, Marburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Barry E.J.</namePart><namePart type="family">Simpson</namePart><affiliation>Institut für Virologie, Justus Liebig Universität, Giessen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wolfgang</namePart><namePart type="family">Garten</namePart><affiliation>Institut für Virologie, Philipps Universität, Marburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hans-Dieter</namePart><namePart type="family">Klenk</namePart><affiliation>To whom requests for reprints should be addressed.</affiliation><affiliation>Institut für Virologie, Philipps Universität, Marburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rudolf</namePart><namePart type="family">Rott</namePart><affiliation>Institut für Virologie, Justus Liebig Universität, Giessen, Germany</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">1989</dateIssued><copyrightDate encoding="w3cdtf">1989</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Six variants that form plaques in chick embryo cells in the absence of trypsin have been isolated from the apathogenic avian influenza virus A/chick/Pennsylvania/l/83 (H5N2). Unlike the wild-type, the plaque variants contain a hemagglutinin that is cleaved in chick embryo cells and MDCK cells. The variants differ also from the wild-type in their pathogenicity for chickens. Nucleotide sequence and oligosaccharide analysis of the hemagglutinin have revealed that, unlike natural isolates with increased pathogenicity (Y. Kawaoka et al., 1984, Virology 139, 303–316; Y. Kawaoka and R. G. Webster, 1985, Virology 146, 130–137), the variants obtained in vitro have retained an oligosaccharide at asparagine 11 that is believed to interfere with the cleavage site of the wild-type. However, all variants showed mutations in the hemagglutinin resulting in an increased number of basic groups at the cleavage site. These observations demonstrate that masking of the cleavage site by an oligosaccharide is overcome by an enhancement of the basic charge at the cleavage site.</abstract><note>Sequence data from this article have been deposited with the EMBUGenBank Data Libraries under Accession No. J04325.</note><relatedItem type="host"><titleInfo><title>Virology</title></titleInfo><titleInfo type="abbreviated"><title>YVIRO</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1989</dateIssued></originInfo><identifier type="ISSN">0042-6822</identifier><identifier type="PII">S0042-6822(00)X0336-4</identifier><part><date>1989</date><detail type="volume"><number>168</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>201</start><end>442</end></extent><extent unit="pages"><start>274</start><end>280</end></extent></part></relatedItem><identifier type="istex">588DD3BADFB27DFD4EC344511B9445C2909310CB</identifier><identifier type="ark">ark:/67375/6H6-8H1FW8ZG-D</identifier><identifier type="DOI">10.1016/0042-6822(89)90267-5</identifier><identifier type="PII">0042-6822(89)90267-5</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:/67375/6H6-8H1FW8ZG-D/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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