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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Adaptation of Influenza A Viruses to Cells Expressing Low Levels of Sialic Acid Leads to Loss of Neuraminidase Activity</title>
<author><name sortKey="Hughes, Mark T" sort="Hughes, Mark T" uniqKey="Hughes M" first="Mark T." last="Hughes">Mark T. Hughes</name>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Mcgregor, Martha" sort="Mcgregor, Martha" uniqKey="Mcgregor M" first="Martha" last="Mcgregor">Martha Mcgregor</name>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Suzuki, Takashi" sort="Suzuki, Takashi" uniqKey="Suzuki T" first="Takashi" last="Suzuki">Takashi Suzuki</name>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Suzuki, Yasuo" sort="Suzuki, Yasuo" uniqKey="Suzuki Y" first="Yasuo" last="Suzuki">Yasuo Suzuki</name>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Kawaoka, Yoshihiro" sort="Kawaoka, Yoshihiro" uniqKey="Kawaoka Y" first="Yoshihiro" last="Kawaoka">Yoshihiro Kawaoka</name>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
</author>
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<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">11264365</idno>
<idno type="pmc">114867</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC114867</idno>
<idno type="RBID">PMC:114867</idno>
<idno type="doi">10.1128/JVI.75.8.3766-3770.2001</idno>
<date when="2001">2001</date>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Adaptation of Influenza A Viruses to Cells Expressing Low Levels of Sialic Acid Leads to Loss of Neuraminidase Activity</title>
<author><name sortKey="Hughes, Mark T" sort="Hughes, Mark T" uniqKey="Hughes M" first="Mark T." last="Hughes">Mark T. Hughes</name>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Mcgregor, Martha" sort="Mcgregor, Martha" uniqKey="Mcgregor M" first="Martha" last="Mcgregor">Martha Mcgregor</name>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Suzuki, Takashi" sort="Suzuki, Takashi" uniqKey="Suzuki T" first="Takashi" last="Suzuki">Takashi Suzuki</name>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Suzuki, Yasuo" sort="Suzuki, Yasuo" uniqKey="Suzuki Y" first="Yasuo" last="Suzuki">Yasuo Suzuki</name>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Kawaoka, Yoshihiro" sort="Kawaoka, Yoshihiro" uniqKey="Kawaoka Y" first="Yoshihiro" last="Kawaoka">Yoshihiro Kawaoka</name>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></nlm:aff>
</affiliation>
<affiliation><nlm:aff id="N0x9bbeb38.0xa1961f0"></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="2001">2001</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Influenza A viruses possess two virion surface proteins, hemagglutinin (HA) and neuraminidase (NA). The HA binds to sialyloligosaccharide viral receptors, while the NA removes sialic acids from the host cell and viral sialyloligosaccarides. Alterations of the HA occur during adaptation of influenza viruses to new host species, as in the 1957 and 1968 influenza pandemics. To gain a better understanding of the contributions of the HA and possibly the NA to this process, we generated cell lines expressing reduced levels of the influenza virus receptor determinant, sialic acid, by selecting Madin-Darby canine kidney cells resistant to a lectin specific for sialic acid linked to galactose by α(2-3) or α(2-6) linkages. One of these cell lines had less than 1/10 as much <italic>N</italic>
-acetylneuraminic acid as its parent cell line. When serially passaged in this cell line, human H3N2 viruses lost sialidase activity due to a large internal deletion in the NA gene, without alteration of the HA gene. These findings indicate that NA mutations can contribute to the adaptation of influenza A virus to new host environments and hence may play a role in the transmission of virus across species.</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">J VIROL</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">11264365</article-id>
<article-id pub-id-type="pmc">114867</article-id>
<article-id pub-id-type="publisher-id">1549</article-id>
<article-id pub-id-type="doi">10.1128/JVI.75.8.3766-3770.2001</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Virus-Cell Interactions</subject>
</subj-group>
</article-categories>
<title-group><article-title>Adaptation of Influenza A Viruses to Cells Expressing Low Levels of Sialic Acid Leads to Loss of Neuraminidase Activity</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Hughes</surname>
<given-names>Mark T.</given-names>
</name>
<xref ref-type="aff" rid="N0x9bbeb38.0xa1961f0">1</xref>
<xref ref-type="aff" rid="N0x9bbeb38.0xa1961f0">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>McGregor</surname>
<given-names>Martha</given-names>
</name>
<xref ref-type="aff" rid="N0x9bbeb38.0xa1961f0">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Suzuki</surname>
<given-names>Takashi</given-names>
</name>
<xref ref-type="aff" rid="N0x9bbeb38.0xa1961f0">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Suzuki</surname>
<given-names>Yasuo</given-names>
</name>
<xref ref-type="aff" rid="N0x9bbeb38.0xa1961f0">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kawaoka</surname>
<given-names>Yoshihiro</given-names>
</name>
<xref ref-type="aff" rid="N0x9bbeb38.0xa1961f0">1</xref>
<xref ref-type="aff" rid="N0x9bbeb38.0xa1961f0">4</xref>
<xref ref-type="author-notes" rid="FN150">*</xref>
</contrib>
</contrib-group>
<aff id="N0x9bbeb38.0xa1961f0"> Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin—Madison, Madison, Wisconsin 53706<sup>1</sup>
; Department of Pathology, University of Tennessee—Memphis, Memphis, Tennessee 38163<sup>2</sup>
; and Department of Biochemistry, University of Shizuoka, School of Pharmaceutical Sciences, Shizuoka-shi 422-8526,<sup>3</sup>
and Institute of Medical Science, University of Tokyo, Tokyo 108-8639,<sup>4</sup>
Japan</aff>
<author-notes><fn id="FN150"><label>*</label>
<p>Corresponding author. Mailing address: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin—Madison, 2015 Linden Dr. West, Madison, WI 53706. Phone: (608) 265-4925. Fax: (608) 265-5622. E-mail: <email>kawaokay@svm.vetmed.wisc.edu</email>
.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><month>4</month>
<year>2001</year>
</pub-date>
<volume>75</volume>
<issue>8</issue>
<fpage>3766</fpage>
<lpage>3770</lpage>
<history><date date-type="received"><day>10</day>
<month>8</month>
<year>2000</year>
</date>
<date date-type="accepted"><day>9</day>
<month>1</month>
<year>2001</year>
</date>
</history>
<copyright-statement>Copyright © 2001, American Society for Microbiology</copyright-statement>
<copyright-year>2001</copyright-year>
<abstract><p>Influenza A viruses possess two virion surface proteins, hemagglutinin (HA) and neuraminidase (NA). The HA binds to sialyloligosaccharide viral receptors, while the NA removes sialic acids from the host cell and viral sialyloligosaccarides. Alterations of the HA occur during adaptation of influenza viruses to new host species, as in the 1957 and 1968 influenza pandemics. To gain a better understanding of the contributions of the HA and possibly the NA to this process, we generated cell lines expressing reduced levels of the influenza virus receptor determinant, sialic acid, by selecting Madin-Darby canine kidney cells resistant to a lectin specific for sialic acid linked to galactose by α(2-3) or α(2-6) linkages. One of these cell lines had less than 1/10 as much <italic>N</italic>
-acetylneuraminic acid as its parent cell line. When serially passaged in this cell line, human H3N2 viruses lost sialidase activity due to a large internal deletion in the NA gene, without alteration of the HA gene. These findings indicate that NA mutations can contribute to the adaptation of influenza A virus to new host environments and hence may play a role in the transmission of virus across species.</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>
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