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<title xml:lang="en">Retroviral Vectors Pseudotyped with Severe Acute Respiratory Syndrome Coronavirus S Protein</title>
<author>
<name sortKey="Giroglou, Tsanan" sort="Giroglou, Tsanan" uniqKey="Giroglou T" first="Tsanan" last="Giroglou">Tsanan Giroglou</name>
<affiliation>
<nlm:aff id="aff1"></nlm:aff>
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<author>
<name sortKey="Cinatl, Jindrich" sort="Cinatl, Jindrich" uniqKey="Cinatl J" first="Jindrich" last="Cinatl">Jindrich Cinatl</name>
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<author>
<name sortKey="Rabenau, Holger" sort="Rabenau, Holger" uniqKey="Rabenau H" first="Holger" last="Rabenau">Holger Rabenau</name>
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<name sortKey="Drosten, Christian" sort="Drosten, Christian" uniqKey="Drosten C" first="Christian" last="Drosten">Christian Drosten</name>
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<name sortKey="Schwalbe, Harald" sort="Schwalbe, Harald" uniqKey="Schwalbe H" first="Harald" last="Schwalbe">Harald Schwalbe</name>
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<author>
<name sortKey="Doerr, Hans Wilhelm" sort="Doerr, Hans Wilhelm" uniqKey="Doerr H" first="Hans Wilhelm" last="Doerr">Hans Wilhelm Doerr</name>
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<author>
<name sortKey="Von Laer, Dorothee" sort="Von Laer, Dorothee" uniqKey="Von Laer D" first="Dorothee" last="Von Laer">Dorothee Von Laer</name>
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<idno type="RBID">PMC:506966</idno>
<idno type="doi">10.1128/JVI.78.17.9007-9015.2004</idno>
<date when="2004">2004</date>
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<title xml:lang="en" level="a" type="main">Retroviral Vectors Pseudotyped with Severe Acute Respiratory Syndrome Coronavirus S Protein</title>
<author>
<name sortKey="Giroglou, Tsanan" sort="Giroglou, Tsanan" uniqKey="Giroglou T" first="Tsanan" last="Giroglou">Tsanan Giroglou</name>
<affiliation>
<nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Cinatl, Jindrich" sort="Cinatl, Jindrich" uniqKey="Cinatl J" first="Jindrich" last="Cinatl">Jindrich Cinatl</name>
<affiliation>
<nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Rabenau, Holger" sort="Rabenau, Holger" uniqKey="Rabenau H" first="Holger" last="Rabenau">Holger Rabenau</name>
<affiliation>
<nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Drosten, Christian" sort="Drosten, Christian" uniqKey="Drosten C" first="Christian" last="Drosten">Christian Drosten</name>
<affiliation>
<nlm:aff id="aff1"></nlm:aff>
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<author>
<name sortKey="Schwalbe, Harald" sort="Schwalbe, Harald" uniqKey="Schwalbe H" first="Harald" last="Schwalbe">Harald Schwalbe</name>
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<nlm:aff id="aff1"></nlm:aff>
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<author>
<name sortKey="Doerr, Hans Wilhelm" sort="Doerr, Hans Wilhelm" uniqKey="Doerr H" first="Hans Wilhelm" last="Doerr">Hans Wilhelm Doerr</name>
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</affiliation>
</author>
<author>
<name sortKey="Von Laer, Dorothee" sort="Von Laer, Dorothee" uniqKey="Von Laer D" first="Dorothee" last="Von Laer">Dorothee Von Laer</name>
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<series>
<title level="j">Journal of Virology</title>
<idno type="ISSN">0022-538X</idno>
<idno type="eISSN">1098-5514</idno>
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<date when="2004">2004</date>
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<div type="abstract" xml:lang="en">
<p>The worldwide outbreak of severe acute respiratory syndrome (SARS) was shown to be associated with a novel coronavirus (CoV) now called SARS CoV. We report here the generation of SARS CoV S protein-pseudotyped murine leukemia virus (MLV) vector particles. The wild-type S protein pseudotyped MLV vectors, although at a low efficiency. Partial deletion of the cytoplasmic tail of S dramatically increased infectivity of pseudotypes, with titers only two- to threefold lower than those of pseudotypes generated in parallel with the vesicular stomatitis virus G protein. S-pseudotyped MLV particles were used to analyze viral tropism. MLV(SARS) pseudotypes and wild-type SARS CoV displayed similar cell types and tissue and host restrictions, indicating that the expression of a functional receptor is the major restraint in permissiveness to SARS CoV infection. Efficient gene transfer could be detected in Vero and CaCo2 cells, whereas the level of gene marking of 293T, HeLa, and HepG2 cells was only slightly above background levels. A cat cell line and a dog cell line were not susceptible. Interestingly, PK-15, a porcine kidney cell line, and primary porcine kidney cells were also highly permissive for SARS S pseudotypes and wild-type SARS CoV. This finding suggests that swine may be susceptible to SARS infection and may be a source for infection of humans. Taken together, these results indicate that MLV(SARS) pseudotypes are highly valuable for functional studies of viral tropism and entry and, in addition, can be a powerful tool for the development of therapeutic entry inhibitors without posing a biohazard to human beings.</p>
</div>
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<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">jvi</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>
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<article-id pub-id-type="pmid">15308697</article-id>
<article-id pub-id-type="pmc">506966</article-id>
<article-id pub-id-type="publisher-id">2673-03</article-id>
<article-id pub-id-type="doi">10.1128/JVI.78.17.9007-9015.2004</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Pathogenesis and Immunity</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Retroviral Vectors Pseudotyped with Severe Acute Respiratory Syndrome Coronavirus S Protein</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Giroglou</surname>
<given-names>Tsanan</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Cinatl</surname>
<given-names>Jindrich</given-names>
<suffix>Jr.</suffix>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Rabenau</surname>
<given-names>Holger</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Drosten</surname>
<given-names>Christian</given-names>
</name>
<xref ref-type="aff" rid="aff1">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Schwalbe</surname>
<given-names>Harald</given-names>
</name>
<xref ref-type="aff" rid="aff1">4</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Doerr</surname>
<given-names>Hans Wilhelm</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>von Laer</surname>
<given-names>Dorothee</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
</contrib-group>
<aff id="aff1">Georg-Speyer-Haus, Institute for Biomedical Research,
<label>1</label>
Institute of Medical Virology, Frankfurt University Medical School,
<label>2</label>
Institut für Organische Chemie, Johann Wolfgang Goethe Universität, Frankfurt,
<label>4</label>
Department of Virology, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany
<label>3</label>
</aff>
<author-notes>
<fn id="cor1">
<label>*</label>
<p>Corresponding author. Mailing address: Georg-Speyer-Haus, Paul-Ehrlich-Strasse 42, 60596 Frankfurt a.M., Germany. Phone: 491724069569. Fax: 496963395297. E-mail:
<email>laer@em.uni-frankfurt.de</email>
.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub">
<month>9</month>
<year>2004</year>
</pub-date>
<volume>78</volume>
<issue>17</issue>
<fpage>9007</fpage>
<lpage>9015</lpage>
<history>
<date date-type="received">
<day>23</day>
<month>12</month>
<year>2003</year>
</date>
<date date-type="accepted">
<day>13</day>
<month>4</month>
<year>2004</year>
</date>
</history>
<copyright-statement>Copyright © 2004, American Society for Microbiology</copyright-statement>
<copyright-year>2004</copyright-year>
<abstract>
<p>The worldwide outbreak of severe acute respiratory syndrome (SARS) was shown to be associated with a novel coronavirus (CoV) now called SARS CoV. We report here the generation of SARS CoV S protein-pseudotyped murine leukemia virus (MLV) vector particles. The wild-type S protein pseudotyped MLV vectors, although at a low efficiency. Partial deletion of the cytoplasmic tail of S dramatically increased infectivity of pseudotypes, with titers only two- to threefold lower than those of pseudotypes generated in parallel with the vesicular stomatitis virus G protein. S-pseudotyped MLV particles were used to analyze viral tropism. MLV(SARS) pseudotypes and wild-type SARS CoV displayed similar cell types and tissue and host restrictions, indicating that the expression of a functional receptor is the major restraint in permissiveness to SARS CoV infection. Efficient gene transfer could be detected in Vero and CaCo2 cells, whereas the level of gene marking of 293T, HeLa, and HepG2 cells was only slightly above background levels. A cat cell line and a dog cell line were not susceptible. Interestingly, PK-15, a porcine kidney cell line, and primary porcine kidney cells were also highly permissive for SARS S pseudotypes and wild-type SARS CoV. This finding suggests that swine may be susceptible to SARS infection and may be a source for infection of humans. Taken together, these results indicate that MLV(SARS) pseudotypes are highly valuable for functional studies of viral tropism and entry and, in addition, can be a powerful tool for the development of therapeutic entry inhibitors without posing a biohazard to human beings.</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>

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