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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Determinant of receptor-preference switch in influenza hemagglutinin</title><author><name sortKey="Ni, Fengyun" sort="Ni, Fengyun" uniqKey="Ni F" first="Fengyun" last="Ni">Fengyun Ni</name><affiliation><nlm:aff id="A1">Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA</nlm:aff></affiliation></author><author><name sortKey="Kondrashkina, Elena" sort="Kondrashkina, Elena" uniqKey="Kondrashkina E" first="Elena" last="Kondrashkina">Elena Kondrashkina</name><affiliation><nlm:aff id="A2">Life Sciences Collaborative Access Team (LS-CAT), Synchrotron Research Center, Northwestern University, Argonne, IL 60439, USA</nlm:aff></affiliation></author><author><name sortKey="Wang, Qinghua" sort="Wang, Qinghua" uniqKey="Wang Q" first="Qinghua" last="Wang">Qinghua Wang</name><affiliation><nlm:aff id="A1">Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">29055255</idno><idno type="pmc">5907505</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5907505</idno><idno type="RBID">PMC:5907505</idno><idno type="doi">10.1016/j.virol.2017.10.010</idno><date when="2017">2017</date><idno type="wicri:Area/Pmc/Corpus">000791</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000791</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Determinant of receptor-preference switch in influenza hemagglutinin</title><author><name sortKey="Ni, Fengyun" sort="Ni, Fengyun" uniqKey="Ni F" first="Fengyun" last="Ni">Fengyun Ni</name><affiliation><nlm:aff id="A1">Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA</nlm:aff></affiliation></author><author><name sortKey="Kondrashkina, Elena" sort="Kondrashkina, Elena" uniqKey="Kondrashkina E" first="Elena" last="Kondrashkina">Elena Kondrashkina</name><affiliation><nlm:aff id="A2">Life Sciences Collaborative Access Team (LS-CAT), Synchrotron Research Center, Northwestern University, Argonne, IL 60439, USA</nlm:aff></affiliation></author><author><name sortKey="Wang, Qinghua" sort="Wang, Qinghua" uniqKey="Wang Q" first="Qinghua" last="Wang">Qinghua Wang</name><affiliation><nlm:aff id="A1">Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Virology</title><idno type="ISSN">0042-6822</idno><idno type="eISSN">1096-0341</idno><imprint><date when="2017">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Influenza pandemic occurs when a new strain from other animal species overcomes the inter-species barriers and supports rapid human-to-human transmission. A critical prerequisite to this process is that hemagglutinin (HA) acquires a few key mutations to switch from avian receptors to human receptors. Previous studies suggest that H1 and H2/H3 HAs use different sets of mutations for the switch. This report shows that HA from the 1918 H1N1 pandemic virus (1918H1 HA) adopts the set of mutations used by H2/H3 HAs in receptor-preference switch when its 130-loop is made similar to those of H2/H3 HAs. Thus, the 130-loop appears to be the key determinant for the different mutations employed by pandemic H1 or H2/H3 HA. The correlation of the mutational routes and the 130-loop as unraveled in this study opens the door for efficient investigation of mutations required by other HA subtypes for inter-human airborne transmission.</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>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">0110674</journal-id><journal-id journal-id-type="pubmed-jr-id">8015</journal-id><journal-id journal-id-type="nlm-ta">Virology</journal-id><journal-id journal-id-type="iso-abbrev">Virology</journal-id><journal-title-group><journal-title>Virology</journal-title></journal-title-group><issn pub-type="ppub">0042-6822</issn><issn pub-type="epub">1096-0341</issn></journal-meta><article-meta><article-id pub-id-type="pmid">29055255</article-id><article-id pub-id-type="pmc">5907505</article-id><article-id pub-id-type="doi">10.1016/j.virol.2017.10.010</article-id><article-id pub-id-type="manuscript">NIHMS914231</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Determinant of receptor-preference switch in influenza hemagglutinin</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Ni</surname><given-names>Fengyun</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Kondrashkina</surname><given-names>Elena</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Qinghua</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1</label>Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA</aff><aff id="A2"><label>2</label>Life Sciences Collaborative Access Team (LS-CAT), Synchrotron Research Center, Northwestern University, Argonne, IL 60439, USA</aff><author-notes><corresp id="FN1">Correspondence and Lead Contact: Qinghua Wang; <email>qinghuaw@bcm.edu</email>; Phone: 713-798-5289; Fax: 713-796-9438</corresp><fn fn-type="COI-statement" id="FN3"><p id="P28"><bold>Conflict of Interest</bold></p><p id="P29">The authors declare no conflict of interest.</p></fn></author-notes><pub-date pub-type="nihms-submitted"><day>9</day><month>11</month><year>2017</year></pub-date><pub-date pub-type="epub"><day>18</day><month>10</month><year>2017</year></pub-date><pub-date pub-type="ppub"><day>01</day><month>1</month><year>2018</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>1</month><year>2019</year></pub-date><volume>513</volume><fpage>98</fpage><lpage>107</lpage><pmc-comment>elocation-id from pubmed: 10.1016/j.virol.2017.10.010</pmc-comment>
<abstract><p id="P1">Influenza pandemic occurs when a new strain from other animal species overcomes the inter-species barriers and supports rapid human-to-human transmission. A critical prerequisite to this process is that hemagglutinin (HA) acquires a few key mutations to switch from avian receptors to human receptors. Previous studies suggest that H1 and H2/H3 HAs use different sets of mutations for the switch. This report shows that HA from the 1918 H1N1 pandemic virus (1918H1 HA) adopts the set of mutations used by H2/H3 HAs in receptor-preference switch when its 130-loop is made similar to those of H2/H3 HAs. Thus, the 130-loop appears to be the key determinant for the different mutations employed by pandemic H1 or H2/H3 HA. The correlation of the mutational routes and the 130-loop as unraveled in this study opens the door for efficient investigation of mutations required by other HA subtypes for inter-human airborne transmission.</p></abstract><kwd-group><kwd>Human adaptation</kwd><kwd>inter-human airborne transmission</kwd><kwd>influenza pandemics</kwd><kwd>receptor binding</kwd><kwd>the 130-loop</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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