1918 Influenza Receptor Binding Domain Variants Bind and Replicate in Primary Human Airway Cells Regardless of Receptor Specificity
Identifieur interne : 000329 ( Pmc/Checkpoint ); précédent : 000328; suivant : 0003301918 Influenza Receptor Binding Domain Variants Bind and Replicate in Primary Human Airway Cells Regardless of Receptor Specificity
Auteurs : A. Sally Davis [États-Unis] ; Daniel S. Chertow [États-Unis] ; Jason Kindrachuk [États-Unis] ; Li Qi [États-Unis] ; Louis M. Schwartzman [États-Unis] ; Jon Suzich [États-Unis] ; Sara Alsaaty [États-Unis] ; Carolea Logun [États-Unis] ; James H. Shelhamer [États-Unis] ; Jeffery K. Taubenberger [États-Unis]Source :
- Virology [ 0042-6822 ] ; 2016.
Abstract
The 1918 influenza pandemic caused ~50 million deaths. Many questions remain regarding the origin, pathogenicity, and mechanisms of human adaptation of this virus. Avian-adapted influenza A viruses preferentially bind α2,3-linked sialic acids (Sia) while human-adapted viruses preferentially bind α2,6-linked Sia. A change in Sia preference from α2,3 to α2,6 is thought to be a requirement for human adaptation of avian influenza viruses. Autopsy data from 1918 cases, however, suggest that factors other than Sia preference played a role in viral binding and entry to human airway cells. Here, we evaluated binding and entry of five 1918 influenza receptor binding domain variants in a primary human airway cell model along with control avian and human influenza viruses. We observed that all five variants bound and entered cells efficiently and that Sia preference did not predict entry of influenza A virus to primary human airway cells evaluated in this model.
Url:
DOI: 10.1016/j.virol.2016.03.025
PubMed: 27062579
PubMed Central: 4949484
Affiliations:
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<front><div type="abstract" xml:lang="en"><p id="P2">The 1918 influenza pandemic caused ~50 million deaths. Many questions remain regarding the origin, pathogenicity, and mechanisms of human adaptation of this virus. Avian-adapted influenza A viruses preferentially bind α2,3-linked sialic acids (Sia) while human-adapted viruses preferentially bind α2,6-linked Sia. A change in Sia preference from α2,3 to α2,6 is thought to be a requirement for human adaptation of avian influenza viruses. Autopsy data from 1918 cases, however, suggest that factors other than Sia preference played a role in viral binding and entry to human airway cells. Here, we evaluated binding and entry of five 1918 influenza receptor binding domain variants in a primary human airway cell model along with control avian and human influenza viruses. We observed that all five variants bound and entered cells efficiently and that Sia preference did not predict entry of influenza A virus to primary human airway cells evaluated in this model.</p>
</div>
</front>
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<title-group><article-title>1918 Influenza Receptor Binding Domain Variants Bind and Replicate in Primary Human Airway Cells Regardless of Receptor Specificity</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Davis</surname>
<given-names>A. Sally</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A2">b</xref>
<xref rid="FN2" ref-type="author-notes">1</xref>
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<contrib contrib-type="author"><name><surname>Chertow</surname>
<given-names>Daniel S.</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A3">c</xref>
<xref rid="FN2" ref-type="author-notes">1</xref>
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<contrib contrib-type="author"><name><surname>Kindrachuk</surname>
<given-names>Jason</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A3">c</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Qi</surname>
<given-names>Li</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Schwartzman</surname>
<given-names>Louis M.</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Suzich</surname>
<given-names>Jon</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A3">c</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Alsaaty</surname>
<given-names>Sara</given-names>
</name>
<xref ref-type="aff" rid="A3">c</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Logun</surname>
<given-names>Carolea</given-names>
</name>
<xref ref-type="aff" rid="A3">c</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Shelhamer</surname>
<given-names>James H.</given-names>
</name>
<xref ref-type="aff" rid="A3">c</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Taubenberger</surname>
<given-names>Jeffery K.</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<xref rid="FN1" ref-type="author-notes">*</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>a</label>
Viral Pathogenesis and Evolution Section, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD</aff>
<aff id="A2"><label>b</label>
Diagnostic Medicine and Pathobiology, Kansas State University College of Veterinary Medicine, Manhattan, KS</aff>
<aff id="A3"><label>c</label>
Critical Care Medicine Department, Clinical Center, NIH, Bethesda, MD</aff>
<author-notes><corresp id="FN1"><label>*</label>
Corresponding author. Jeffery K. Taubenberger, M.D., Ph.D., NIAID, 33 North Dr., MSC 3203, Bethesda, MD 20892; Phone: (301) 443-5960; Fax: (301) 480-1696; <email>taubenbergerj@niaid.nih.gov</email>
</corresp>
<fn id="FN2" fn-type="equal"><label>1</label>
<p>These authors contributed equally to this manuscript.</p>
</fn>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>12</day>
<month>7</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub"><day>11</day>
<month>4</month>
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<pub-date pub-type="ppub"><month>6</month>
<year>2016</year>
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<pub-date pub-type="pmc-release"><day>01</day>
<month>6</month>
<year>2017</year>
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<fpage>238</fpage>
<lpage>246</lpage>
<pmc-comment>elocation-id from pubmed: 10.1016/j.virol.2016.03.025</pmc-comment>
<abstract><p id="P2">The 1918 influenza pandemic caused ~50 million deaths. Many questions remain regarding the origin, pathogenicity, and mechanisms of human adaptation of this virus. Avian-adapted influenza A viruses preferentially bind α2,3-linked sialic acids (Sia) while human-adapted viruses preferentially bind α2,6-linked Sia. A change in Sia preference from α2,3 to α2,6 is thought to be a requirement for human adaptation of avian influenza viruses. Autopsy data from 1918 cases, however, suggest that factors other than Sia preference played a role in viral binding and entry to human airway cells. Here, we evaluated binding and entry of five 1918 influenza receptor binding domain variants in a primary human airway cell model along with control avian and human influenza viruses. We observed that all five variants bound and entered cells efficiently and that Sia preference did not predict entry of influenza A virus to primary human airway cells evaluated in this model.</p>
</abstract>
<kwd-group><kwd>Influenza A virus</kwd>
<kwd>Pandemic</kwd>
<kwd>Receptor binding</kwd>
<kwd>hemagglutinin</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Kansas</li>
<li>Maryland</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Maryland"><name sortKey="Davis, A Sally" sort="Davis, A Sally" uniqKey="Davis A" first="A. Sally" last="Davis">A. Sally Davis</name>
</region>
<name sortKey="Alsaaty, Sara" sort="Alsaaty, Sara" uniqKey="Alsaaty S" first="Sara" last="Alsaaty">Sara Alsaaty</name>
<name sortKey="Chertow, Daniel S" sort="Chertow, Daniel S" uniqKey="Chertow D" first="Daniel S." last="Chertow">Daniel S. Chertow</name>
<name sortKey="Chertow, Daniel S" sort="Chertow, Daniel S" uniqKey="Chertow D" first="Daniel S." last="Chertow">Daniel S. Chertow</name>
<name sortKey="Davis, A Sally" sort="Davis, A Sally" uniqKey="Davis A" first="A. Sally" last="Davis">A. Sally Davis</name>
<name sortKey="Kindrachuk, Jason" sort="Kindrachuk, Jason" uniqKey="Kindrachuk J" first="Jason" last="Kindrachuk">Jason Kindrachuk</name>
<name sortKey="Kindrachuk, Jason" sort="Kindrachuk, Jason" uniqKey="Kindrachuk J" first="Jason" last="Kindrachuk">Jason Kindrachuk</name>
<name sortKey="Logun, Carolea" sort="Logun, Carolea" uniqKey="Logun C" first="Carolea" last="Logun">Carolea Logun</name>
<name sortKey="Qi, Li" sort="Qi, Li" uniqKey="Qi L" first="Li" last="Qi">Li Qi</name>
<name sortKey="Schwartzman, Louis M" sort="Schwartzman, Louis M" uniqKey="Schwartzman L" first="Louis M." last="Schwartzman">Louis M. Schwartzman</name>
<name sortKey="Shelhamer, James H" sort="Shelhamer, James H" uniqKey="Shelhamer J" first="James H." last="Shelhamer">James H. Shelhamer</name>
<name sortKey="Suzich, Jon" sort="Suzich, Jon" uniqKey="Suzich J" first="Jon" last="Suzich">Jon Suzich</name>
<name sortKey="Suzich, Jon" sort="Suzich, Jon" uniqKey="Suzich J" first="Jon" last="Suzich">Jon Suzich</name>
<name sortKey="Taubenberger, Jeffery K" sort="Taubenberger, Jeffery K" uniqKey="Taubenberger J" first="Jeffery K." last="Taubenberger">Jeffery K. Taubenberger</name>
</country>
</tree>
</affiliations>
</record>
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