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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Cooperation between the Hemagglutinin of Avian Viruses and the Matrix Protein of Human Influenza A Viruses</title><author><name sortKey="Scholtissek, Christoph" sort="Scholtissek, Christoph" uniqKey="Scholtissek C" first="Christoph" last="Scholtissek">Christoph Scholtissek</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Stech, Jurgen" sort="Stech, Jurgen" uniqKey="Stech J" first="Jürgen" last="Stech">Jürgen Stech</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Krauss, Scott" sort="Krauss, Scott" uniqKey="Krauss S" first="Scott" last="Krauss">Scott Krauss</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Webster, Robert G" sort="Webster, Robert G" uniqKey="Webster R" first="Robert G." last="Webster">Robert G. Webster</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">11799173</idno><idno type="pmc">135889</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC135889</idno><idno type="RBID">PMC:135889</idno><idno type="doi">10.1128/JVI.76.4.1781-1786.2002</idno><date when="2002">2002</date><idno type="wicri:Area/Pmc/Corpus">000373</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000373</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Cooperation between the Hemagglutinin of Avian Viruses and the Matrix Protein of Human Influenza A Viruses</title><author><name sortKey="Scholtissek, Christoph" sort="Scholtissek, Christoph" uniqKey="Scholtissek C" first="Christoph" last="Scholtissek">Christoph Scholtissek</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Stech, Jurgen" sort="Stech, Jurgen" uniqKey="Stech J" first="Jürgen" last="Stech">Jürgen Stech</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Krauss, Scott" sort="Krauss, Scott" uniqKey="Krauss S" first="Scott" last="Krauss">Scott Krauss</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Webster, Robert G" sort="Webster, Robert G" uniqKey="Webster R" first="Robert G." last="Webster">Robert G. Webster</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Virology</title><idno type="ISSN">0022-538X</idno><idno type="eISSN">1098-5514</idno><imprint><date when="2002">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>To analyze the compatibility of avian influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M) proteins M1 and M2, we doubly infected Madin-Darby canine kidney cells with amantadine (1-aminoadamantane hydrochloride)-resistant human viruses and amantadine-sensitive avian strains. By using antisera against the human virus HAs and amantadine, we selected reassortants containing the human virus M gene and the avian virus HA gene. In our system, high virus yields and large, well-defined plaques indicated that the avian HAs and the human M gene products could cooperate effectively; low virus yields and small, turbid plaques indicated that cooperation was poor. The M gene products are among the primary components that determine the species specificities of influenza A viruses. Therefore, our system also indicated whether the avian HA genes effectively reassorted into the genome and replaced the HA gene of the prevailing human influenza A viruses. Most of the avian HAs that we tested efficiently cooperated with the M gene products of the early human A/PR/8/34 (H1N1) virus; however, the avian HAs did not effectively cooperate with the most recently isolated human virus that we tested, A/Nanchang/933/95 (H3N2). Cooperation between the avian HAs and the M proteins of the human A/Singapore/57 (H2N2) virus was moderate. These results suggest that the currently prevailing human influenza A viruses might have lost their ability to undergo antigenic shift and therefore are unable to form new pandemic viruses that contain an avian HA, a finding that is of great interest for pandemic planning.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Virol</journal-id><journal-id journal-id-type="publisher-id">jvi</journal-id><journal-title>Journal of Virology</journal-title><issn pub-type="ppub">0022-538X</issn><issn pub-type="epub">1098-5514</issn><publisher><publisher-name>American Society for Microbiology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">11799173</article-id><article-id pub-id-type="pmc">135889</article-id><article-id pub-id-type="publisher-id">1355</article-id><article-id pub-id-type="doi">10.1128/JVI.76.4.1781-1786.2002</article-id><article-categories><subj-group subj-group-type="heading"><subject>Virus-Cell Interactions</subject></subj-group></article-categories><title-group><article-title>Cooperation between the Hemagglutinin of Avian Viruses and the Matrix Protein of Human Influenza A Viruses</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Scholtissek</surname><given-names>Christoph</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="fn" rid="fn1">†</xref></contrib><contrib contrib-type="author"><name><surname>Stech</surname><given-names>Jürgen</given-names></name><xref ref-type="aff" rid="aff1">2</xref></contrib><contrib contrib-type="author"><name><surname>Krauss</surname><given-names>Scott</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Webster</surname><given-names>Robert G.</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff1">3</xref><xref ref-type="corresp" rid="cor1">*</xref></contrib></contrib-group><aff id="aff1">Departments of Virology,<label>1</label> Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794 ,<label>3</label> Institute of Virology, Philipps University Marburg, D-35032 Marburg, Germany<label>2</label></aff><author-notes><fn id="cor1"><label>*</label><p>Corresponding author. Mailing address: Department of Virology, St. Jude Children's Research Hospital, 332 N. Lauderdale, Memphis, TN 38105-2794. Phone: (901) 495-3400. Fax: (901) 523-2622. E-mail: <email>robert.webster@stjude.org</email>.</p></fn><fn id="fn1"><label>†</label><p>Present address: Waldstrasse 53, D-35440 Linden, Germany.</p></fn></author-notes><pub-date pub-type="ppub"><month>2</month><year>2002</year></pub-date><volume>76</volume><issue>4</issue><fpage>1781</fpage><lpage>1786</lpage><history><date date-type="received"><day>12</day><month>7</month><year>2001</year></date><date date-type="accepted"><day>1</day><month>11</month><year>2001</year></date></history><copyright-year>2002</copyright-year><abstract><p>To analyze the compatibility of avian influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M) proteins M1 and M2, we doubly infected Madin-Darby canine kidney cells with amantadine (1-aminoadamantane hydrochloride)-resistant human viruses and amantadine-sensitive avian strains. By using antisera against the human virus HAs and amantadine, we selected reassortants containing the human virus M gene and the avian virus HA gene. In our system, high virus yields and large, well-defined plaques indicated that the avian HAs and the human M gene products could cooperate effectively; low virus yields and small, turbid plaques indicated that cooperation was poor. The M gene products are among the primary components that determine the species specificities of influenza A viruses. Therefore, our system also indicated whether the avian HA genes effectively reassorted into the genome and replaced the HA gene of the prevailing human influenza A viruses. Most of the avian HAs that we tested efficiently cooperated with the M gene products of the early human A/PR/8/34 (H1N1) virus; however, the avian HAs did not effectively cooperate with the most recently isolated human virus that we tested, A/Nanchang/933/95 (H3N2). Cooperation between the avian HAs and the M proteins of the human A/Singapore/57 (H2N2) virus was moderate. These results suggest that the currently prevailing human influenza A viruses might have lost their ability to undergo antigenic shift and therefore are unable to form new pandemic viruses that contain an avian HA, a finding that is of great interest for pandemic planning.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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