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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>
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