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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Avian influenza virus hemagglutinins H2, H4, H8, and H14 support a highly pathogenic phenotype</title><author><name sortKey="Veits, Jutta" sort="Veits, Jutta" uniqKey="Veits J" first="Jutta" last="Veits">Jutta Veits</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Weber, Siegfried" sort="Weber, Siegfried" uniqKey="Weber S" first="Siegfried" last="Weber">Siegfried Weber</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Stech, Olga" sort="Stech, Olga" uniqKey="Stech O" first="Olga" last="Stech">Olga Stech</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Breithaupt, Angele" sort="Breithaupt, Angele" uniqKey="Breithaupt A" first="Angele" last="Breithaupt">Angele Breithaupt</name><affiliation><nlm:aff id="aff2">Department of Experimental Animal Facilities and Biorisk Management,<institution>Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health</institution>, 17493 Greifswald-Insel Riems,<country>Germany</country></nlm:aff></affiliation></author><author><name sortKey="Gr Ber, Marcus" sort="Gr Ber, Marcus" uniqKey="Gr Ber M" first="Marcus" last="Gr Ber">Marcus Gr Ber</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Gohrbandt, Sandra" sort="Gohrbandt, Sandra" uniqKey="Gohrbandt S" first="Sandra" last="Gohrbandt">Sandra Gohrbandt</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Bogs, Jessica" sort="Bogs, Jessica" uniqKey="Bogs J" first="Jessica" last="Bogs">Jessica Bogs</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Hundt, Jana" sort="Hundt, Jana" uniqKey="Hundt J" first="Jana" last="Hundt">Jana Hundt</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Teifke, Jens P" sort="Teifke, Jens P" uniqKey="Teifke J" first="Jens P." last="Teifke">Jens P. Teifke</name><affiliation><nlm:aff id="aff2">Department of Experimental Animal Facilities and Biorisk Management,<institution>Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health</institution>, 17493 Greifswald-Insel Riems,<country>Germany</country></nlm:aff></affiliation></author><author><name sortKey="Mettenleiter, Thomas C" sort="Mettenleiter, Thomas C" uniqKey="Mettenleiter T" first="Thomas C." last="Mettenleiter">Thomas C. Mettenleiter</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</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 wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22308331</idno><idno type="pmc">3289369</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3289369</idno><idno type="RBID">PMC:3289369</idno><idno type="doi">10.1073/pnas.1109397109</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">000755</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000755</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Avian influenza virus hemagglutinins H2, H4, H8, and H14 support a highly pathogenic phenotype</title><author><name sortKey="Veits, Jutta" sort="Veits, Jutta" uniqKey="Veits J" first="Jutta" last="Veits">Jutta Veits</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Weber, Siegfried" sort="Weber, Siegfried" uniqKey="Weber S" first="Siegfried" last="Weber">Siegfried Weber</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Stech, Olga" sort="Stech, Olga" uniqKey="Stech O" first="Olga" last="Stech">Olga Stech</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Breithaupt, Angele" sort="Breithaupt, Angele" uniqKey="Breithaupt A" first="Angele" last="Breithaupt">Angele Breithaupt</name><affiliation><nlm:aff id="aff2">Department of Experimental Animal Facilities and Biorisk Management,<institution>Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health</institution>, 17493 Greifswald-Insel Riems,<country>Germany</country></nlm:aff></affiliation></author><author><name sortKey="Gr Ber, Marcus" sort="Gr Ber, Marcus" uniqKey="Gr Ber M" first="Marcus" last="Gr Ber">Marcus Gr Ber</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Gohrbandt, Sandra" sort="Gohrbandt, Sandra" uniqKey="Gohrbandt S" first="Sandra" last="Gohrbandt">Sandra Gohrbandt</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Bogs, Jessica" sort="Bogs, Jessica" uniqKey="Bogs J" first="Jessica" last="Bogs">Jessica Bogs</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Hundt, Jana" sort="Hundt, Jana" uniqKey="Hundt J" first="Jana" last="Hundt">Jana Hundt</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Teifke, Jens P" sort="Teifke, Jens P" uniqKey="Teifke J" first="Jens P." last="Teifke">Jens P. Teifke</name><affiliation><nlm:aff id="aff2">Department of Experimental Animal Facilities and Biorisk Management,<institution>Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health</institution>, 17493 Greifswald-Insel Riems,<country>Germany</country></nlm:aff></affiliation></author><author><name sortKey="Mettenleiter, Thomas C" sort="Mettenleiter, Thomas C" uniqKey="Mettenleiter T" first="Thomas C." last="Mettenleiter">Thomas C. Mettenleiter</name><affiliation><nlm:aff wicri:cut=" and" id="aff1">Institute of Molecular Biology</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 wicri:cut=" and" id="aff1">Institute of Molecular Biology</nlm:aff></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="ISSN">0027-8424</idno><idno type="eISSN">1091-6490</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>High-pathogenic avian influenza viruses (HPAIVs) evolve from low-pathogenic precursors specifying the HA serotypes H5 or H7 by acquisition of a polybasic HA cleavage site. As the reason for this serotype restriction has remained unclear, we aimed to distinguish between compatibility of a polybasic cleavage site with H5/H7 HA only and unique predisposition of these two serotypes for insertion mutations. To this end, we introduced a polybasic cleavage site into the HA of several low-pathogenic avian strains with serotypes H1, H2, H3, H4, H6, H8, H10, H11, H14, or H15, and rescued HA reassortants after cotransfection with the genes from either a low-pathogenic H9N2 or high-pathogenic H5N1 strain. Oculonasal inoculation with those reassortants resulted in varying pathogenicity in chicken. Recombinants containing the engineered H2, H4, H8, or H14 in the HPAIV background were lethal and exhibited i.v. pathogenicity indices of 2.79, 2.37, 2.85, and 2.61, respectively, equivalent to naturally occurring H5 or H7 HPAIV. Moreover, the H2, H4, and H8 reassortants were transmitted to some contact chickens. The H2 reassortant gained two mutations in the M2 proton channel gate region, which is affected in some HPAIVs of various origins. Taken together, in the presence of a polybasic HA cleavage site, non-H5/H7 HA can support a highly pathogenic phenotype in the appropriate viral background, indicating requirement for further adaptation. Therefore, the restriction of natural HPAIV to serotypes H5 and H7 is likely a result of their unique predisposition for acquisition of a polybasic HA cleavage site.</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">Proc Natl Acad Sci U S A</journal-id><journal-id journal-id-type="iso-abbrev">Proc. Natl. Acad. Sci. U.S.A</journal-id><journal-id journal-id-type="hwp">pnas</journal-id><journal-id journal-id-type="pmc">pnas</journal-id><journal-id journal-id-type="publisher-id">PNAS</journal-id><journal-title-group><journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title></journal-title-group><issn pub-type="ppub">0027-8424</issn><issn pub-type="epub">1091-6490</issn><publisher><publisher-name>National Academy of Sciences</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">22308331</article-id><article-id pub-id-type="pmc">3289369</article-id><article-id pub-id-type="publisher-id">201109397</article-id><article-id pub-id-type="doi">10.1073/pnas.1109397109</article-id><article-categories><subj-group subj-group-type="heading"><subject>Biological Sciences</subject><subj-group><subject>Microbiology</subject></subj-group></subj-group></article-categories><title-group><article-title>Avian influenza virus hemagglutinins H2, H4, H8, and H14 support a highly pathogenic phenotype</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Veits</surname><given-names>Jutta</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="author-notes" rid="fn1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Weber</surname><given-names>Siegfried</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="author-notes" rid="fn1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Stech</surname><given-names>Olga</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Breithaupt</surname><given-names>Angele</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Gräber</surname><given-names>Marcus</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Gohrbandt</surname><given-names>Sandra</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="author-notes" rid="fn2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Bogs</surname><given-names>Jessica</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Hundt</surname><given-names>Jana</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="author-notes" rid="fn3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Teifke</surname><given-names>Jens P.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Mettenleiter</surname><given-names>Thomas C.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Stech</surname><given-names>Jürgen</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="corresp" rid="cor1"><sup>4</sup></xref></contrib><aff id="aff1"><sup>a</sup>Institute of Molecular Biology and</aff><aff id="aff2"><sup>b</sup>Department of Experimental Animal Facilities and Biorisk Management,<institution>Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health</institution>, 17493 Greifswald-Insel Riems,<country>Germany</country></aff></contrib-group><author-notes><corresp id="cor1"><sup>4</sup>To whom correspondence should be addressed. E-mail: <email>juergen.stech@fli.bund.de</email>.</corresp><fn fn-type="edited-by"><p>Edited by Peter Palese, Mount Sinai School of Medicine, New York, NY, and approved December 30, 2011 (received for review June 10, 2011)</p></fn><fn fn-type="con"><p>Author contributions: J.V., O.S., A.B., T.C.M., and J.S. designed research; J.V., S.W., O.S., A.B., M.G., S.G., J.B., J.H., and J.S. performed research; J.V., S.W., O.S., A.B., J.P.T., T.C.M., and J.S. analyzed data; and T.C.M. and J.S. wrote the paper.</p></fn><fn id="fn1" fn-type="equal"><p><sup>1</sup>J.V. and S.W. contributed equally to this work.</p></fn><fn id="fn2" fn-type="present-address"><p><sup>2</sup>Present address: Institute of Immunology, Laboratoire National de Santé, 11 L-1950 Luxembourg.</p></fn><fn id="fn3" fn-type="present-address"><p><sup>3</sup>Present address: Vaccine and Infectious Disease Organization (VIDO)–International Vaccine Centre, Saskatoon, SK, Canada S7N 5E3.</p></fn><fn fn-type="conflict"><p>The authors declare no conflict of interest.</p></fn></author-notes><pub-date pub-type="ppub"><day>14</day><month>2</month><year>2012</year></pub-date><pub-date pub-type="epub"><day>30</day><month>1</month><year>2012</year></pub-date><volume>109</volume><issue>7</issue><fpage>2579</fpage><lpage>2584</lpage><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="pnas.201109397.pdf"></self-uri><abstract><p>High-pathogenic avian influenza viruses (HPAIVs) evolve from low-pathogenic precursors specifying the HA serotypes H5 or H7 by acquisition of a polybasic HA cleavage site. As the reason for this serotype restriction has remained unclear, we aimed to distinguish between compatibility of a polybasic cleavage site with H5/H7 HA only and unique predisposition of these two serotypes for insertion mutations. To this end, we introduced a polybasic cleavage site into the HA of several low-pathogenic avian strains with serotypes H1, H2, H3, H4, H6, H8, H10, H11, H14, or H15, and rescued HA reassortants after cotransfection with the genes from either a low-pathogenic H9N2 or high-pathogenic H5N1 strain. Oculonasal inoculation with those reassortants resulted in varying pathogenicity in chicken. Recombinants containing the engineered H2, H4, H8, or H14 in the HPAIV background were lethal and exhibited i.v. pathogenicity indices of 2.79, 2.37, 2.85, and 2.61, respectively, equivalent to naturally occurring H5 or H7 HPAIV. Moreover, the H2, H4, and H8 reassortants were transmitted to some contact chickens. The H2 reassortant gained two mutations in the M2 proton channel gate region, which is affected in some HPAIVs of various origins. Taken together, in the presence of a polybasic HA cleavage site, non-H5/H7 HA can support a highly pathogenic phenotype in the appropriate viral background, indicating requirement for further adaptation. Therefore, the restriction of natural HPAIV to serotypes H5 and H7 is likely a result of their unique predisposition for acquisition of a polybasic HA cleavage site.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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