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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Retargeting of Coronavirus by Substitution of the Spike Glycoprotein Ectodomain: Crossing the Host Cell Species Barrier</title>
<author><name sortKey="Kuo, Lili" sort="Kuo, Lili" uniqKey="Kuo L" first="Lili" last="Kuo">Lili Kuo</name>
<affiliation><nlm:aff id="N0x977b4b8.0x994b3d8"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Godeke, Gert Jan" sort="Godeke, Gert Jan" uniqKey="Godeke G" first="Gert-Jan" last="Godeke">Gert-Jan Godeke</name>
<affiliation><nlm:aff id="N0x977b4b8.0x994b3d8"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Raamsman, Martin J B" sort="Raamsman, Martin J B" uniqKey="Raamsman M" first="Martin J. B." last="Raamsman">Martin J. B. Raamsman</name>
<affiliation><nlm:aff id="N0x977b4b8.0x994b3d8"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Masters, Paul S" sort="Masters, Paul S" uniqKey="Masters P" first="Paul S." last="Masters">Paul S. Masters</name>
<affiliation><nlm:aff id="N0x977b4b8.0x994b3d8"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Rottier, Peter J M" sort="Rottier, Peter J M" uniqKey="Rottier P" first="Peter J. M." last="Rottier">Peter J. M. Rottier</name>
<affiliation><nlm:aff id="N0x977b4b8.0x994b3d8"></nlm:aff>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">10627550</idno>
<idno type="pmc">111474</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC111474</idno>
<idno type="RBID">PMC:111474</idno>
<date when="2000">2000</date>
<idno type="wicri:Area/Pmc/Corpus">000150</idno>
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</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Retargeting of Coronavirus by Substitution of the Spike Glycoprotein Ectodomain: Crossing the Host Cell Species Barrier</title>
<author><name sortKey="Kuo, Lili" sort="Kuo, Lili" uniqKey="Kuo L" first="Lili" last="Kuo">Lili Kuo</name>
<affiliation><nlm:aff id="N0x977b4b8.0x994b3d8"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Godeke, Gert Jan" sort="Godeke, Gert Jan" uniqKey="Godeke G" first="Gert-Jan" last="Godeke">Gert-Jan Godeke</name>
<affiliation><nlm:aff id="N0x977b4b8.0x994b3d8"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Raamsman, Martin J B" sort="Raamsman, Martin J B" uniqKey="Raamsman M" first="Martin J. B." last="Raamsman">Martin J. B. Raamsman</name>
<affiliation><nlm:aff id="N0x977b4b8.0x994b3d8"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Masters, Paul S" sort="Masters, Paul S" uniqKey="Masters P" first="Paul S." last="Masters">Paul S. Masters</name>
<affiliation><nlm:aff id="N0x977b4b8.0x994b3d8"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Rottier, Peter J M" sort="Rottier, Peter J M" uniqKey="Rottier P" first="Peter J. M." last="Rottier">Peter J. M. Rottier</name>
<affiliation><nlm:aff id="N0x977b4b8.0x994b3d8"></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="2000">2000</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Coronaviruses generally have a narrow host range, infecting one or just a few species. Using targeted RNA recombination, we constructed a mutant of the coronavirus mouse hepatitis virus (MHV) in which the ectodomain of the spike glycoprotein (S) was replaced with the highly divergent ectodomain of the S protein of feline infectious peritonitis virus. The resulting chimeric virus, designated fMHV, acquired the ability to infect feline cells and simultaneously lost the ability to infect murine cells in tissue culture. This reciprocal switch of species specificity strongly supports the notion that coronavirus host cell range is determined primarily at the level of interactions between the S protein and the virus receptor. The isolation of fMHV allowed the localization of the region responsible for S protein incorporation into virions to the carboxy-terminal 64 of the 1,324 residues of this protein. This establishes a basis for further definition of elements involved in virion assembly. In addition, fMHV is potentially the ideal recipient virus for carrying out reverse genetics of MHV by targeted RNA recombination, since it presents the possibility of selecting recombinants, no matter how defective, that have regained the ability to replicate in murine cells.</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">10627550</article-id>
<article-id pub-id-type="pmc">111474</article-id>
<article-id pub-id-type="publisher-id">1167</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Structure and Assembly</subject>
</subj-group>
</article-categories>
<title-group><article-title>Retargeting of Coronavirus by Substitution of the Spike Glycoprotein Ectodomain: Crossing the Host Cell Species Barrier</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Kuo</surname>
<given-names>Lili</given-names>
</name>
<xref ref-type="aff" rid="N0x977b4b8.0x994b3d8">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Godeke</surname>
<given-names>Gert-Jan</given-names>
</name>
<xref ref-type="aff" rid="N0x977b4b8.0x994b3d8">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Raamsman</surname>
<given-names>Martin J. B.</given-names>
</name>
<xref ref-type="aff" rid="N0x977b4b8.0x994b3d8">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Masters</surname>
<given-names>Paul S.</given-names>
</name>
<xref ref-type="aff" rid="N0x977b4b8.0x994b3d8">1</xref>
<xref ref-type="author-notes" rid="FN150">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Rottier</surname>
<given-names>Peter J. M.</given-names>
</name>
<xref ref-type="aff" rid="N0x977b4b8.0x994b3d8">2</xref>
</contrib>
</contrib-group>
<aff id="N0x977b4b8.0x994b3d8"> David Axelrod Institute, Wadsworth Center for Laboratories and Research, New York State Department of Health, Albany, New York 12201,<sup>1</sup>
and Institute of Virology, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, and Institute of Biomembranes, Utrecht University, 3584 CL Utrecht, The Netherlands<sup>2</sup>
</aff>
<author-notes><fn id="FN150"><label>*</label>
<p>Corresponding author. Mailing address: David Axelrod Institute, Wadsworth Center, NYSDOH, New Scotland Ave., P.O. Box 22002, Albany, NY 12201-2002. Phone: (518) 474-1283. Fax: (518) 473-1326. E-mail: <email>masters@wadsworth.org</email>
.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><month>2</month>
<year>2000</year>
</pub-date>
<volume>74</volume>
<issue>3</issue>
<fpage>1393</fpage>
<lpage>1406</lpage>
<history><date date-type="received"><day>8</day>
<month>7</month>
<year>1999</year>
</date>
<date date-type="accepted"><day>25</day>
<month>10</month>
<year>1999</year>
</date>
</history>
<copyright-statement>Copyright © 2000, American Society for Microbiology</copyright-statement>
<copyright-year>2000</copyright-year>
<abstract><p>Coronaviruses generally have a narrow host range, infecting one or just a few species. Using targeted RNA recombination, we constructed a mutant of the coronavirus mouse hepatitis virus (MHV) in which the ectodomain of the spike glycoprotein (S) was replaced with the highly divergent ectodomain of the S protein of feline infectious peritonitis virus. The resulting chimeric virus, designated fMHV, acquired the ability to infect feline cells and simultaneously lost the ability to infect murine cells in tissue culture. This reciprocal switch of species specificity strongly supports the notion that coronavirus host cell range is determined primarily at the level of interactions between the S protein and the virus receptor. The isolation of fMHV allowed the localization of the region responsible for S protein incorporation into virions to the carboxy-terminal 64 of the 1,324 residues of this protein. This establishes a basis for further definition of elements involved in virion assembly. In addition, fMHV is potentially the ideal recipient virus for carrying out reverse genetics of MHV by targeted RNA recombination, since it presents the possibility of selecting recombinants, no matter how defective, that have regained the ability to replicate in murine cells.</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>
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