A Severe Acute Respiratory Syndrome-Associated Coronavirus-Specific Protein Enhances Virulence of an Attenuated Murine Coronavirus
Identifieur interne : 000696 ( Pmc/Corpus ); précédent : 000695; suivant : 000697A Severe Acute Respiratory Syndrome-Associated Coronavirus-Specific Protein Enhances Virulence of an Attenuated Murine Coronavirus
Auteurs : Lecia Pewe ; Haixia Zhou ; Jason Netland ; Chandra Tangudu ; Heidi Olivares ; Lei Shi ; Dwight Look ; Thomas Gallagher ; Stanley PerlmanSource :
- Journal of Virology [ 0022-538X ] ; 2005.
Abstract
Most animal species that can be infected with the severe acute respiratory syndrome-associated coronavirus (SARS-CoV) do not reproducibly develop clinical disease, hindering studies of pathogenesis. To develop an alternative system for the study of SARS-CoV, we introduced individual SARS-CoV genes (open reading frames [ORFs]) into the genome of an attenuated murine coronavirus. One protein, the product of SARS-CoV ORF6, converted a sublethal infection to a uniformly lethal encephalitis and enhanced virus growth in tissue culture cells, indicating that SARS-CoV proteins function in the context of a heterologous coronavirus infection. Furthermore, these results suggest that the attenuated murine coronavirus lacks a virulence gene residing in SARS-CoV. Recombinant murine coronaviruses cause a reproducible and well-characterized clinical disease, offer virtually no risk to laboratory personnel, and should be useful for elucidating the role of SARS-CoV nonstructural proteins in viral replication and pathogenesis.
Url:
DOI: 10.1128/JVI.79.17.11335-11342.2005
PubMed: 16103185
PubMed Central: 1193615
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PMC:1193615Le document en format XML
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uniqKey="Zhou H" first="Haixia" last="Zhou">Haixia Zhou</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Netland, Jason" sort="Netland, Jason" uniqKey="Netland J" first="Jason" last="Netland">Jason Netland</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Tangudu, Chandra" sort="Tangudu, Chandra" uniqKey="Tangudu C" first="Chandra" last="Tangudu">Chandra Tangudu</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Olivares, Heidi" sort="Olivares, Heidi" uniqKey="Olivares H" first="Heidi" last="Olivares">Heidi Olivares</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Shi, Lei" sort="Shi, Lei" uniqKey="Shi L" first="Lei" last="Shi">Lei Shi</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Look, Dwight" sort="Look, Dwight" uniqKey="Look D" first="Dwight" last="Look">Dwight Look</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Gallagher, Thomas" sort="Gallagher, Thomas" uniqKey="Gallagher T" first="Thomas" last="Gallagher">Thomas Gallagher</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></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="2005">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Most animal species that can be infected with the severe acute respiratory syndrome-associated coronavirus (SARS-CoV) do not reproducibly develop clinical disease, hindering studies of pathogenesis. To develop an alternative system for the study of SARS-CoV, we introduced individual SARS-CoV genes (open reading frames [ORFs]) into the genome of an attenuated murine coronavirus. One protein, the product of SARS-CoV ORF6, converted a sublethal infection to a uniformly lethal encephalitis and enhanced virus growth in tissue culture cells, indicating that SARS-CoV proteins function in the context of a heterologous coronavirus infection. Furthermore, these results suggest that the attenuated murine coronavirus lacks a virulence gene residing in SARS-CoV. Recombinant murine coronaviruses cause a reproducible and well-characterized clinical disease, offer virtually no risk to laboratory personnel, and should be useful for elucidating the role of SARS-CoV nonstructural proteins in viral replication and pathogenesis.</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">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></journal-meta><article-meta><article-id pub-id-type="pmid">16103185</article-id><article-id pub-id-type="pmc">1193615</article-id><article-id pub-id-type="publisher-id">0734-05</article-id><article-id pub-id-type="doi">10.1128/JVI.79.17.11335-11342.2005</article-id><article-categories><subj-group subj-group-type="heading"><subject>Pathogenesis and Immunity</subject></subj-group></article-categories><title-group><article-title>A Severe Acute Respiratory Syndrome-Associated Coronavirus-Specific Protein Enhances Virulence of an Attenuated Murine Coronavirus</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Pewe</surname><given-names>Lecia</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="fn" rid="fn1">†</xref></contrib><contrib contrib-type="author"><name><surname>Zhou</surname><given-names>Haixia</given-names></name><xref ref-type="aff" rid="aff1">2</xref><xref ref-type="fn" rid="fn1">†</xref></contrib><contrib contrib-type="author"><name><surname>Netland</surname><given-names>Jason</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Tangudu</surname><given-names>Chandra</given-names></name><xref ref-type="aff" rid="aff1">3</xref></contrib><contrib contrib-type="author"><name><surname>Olivares</surname><given-names>Heidi</given-names></name><xref ref-type="aff" rid="aff1">3</xref></contrib><contrib contrib-type="author"><name><surname>Shi</surname><given-names>Lei</given-names></name><xref ref-type="aff" rid="aff1">4</xref></contrib><contrib contrib-type="author"><name><surname>Look</surname><given-names>Dwight</given-names></name><xref ref-type="aff" rid="aff1">4</xref></contrib><contrib contrib-type="author"><name><surname>Gallagher</surname><given-names>Thomas</given-names></name><xref ref-type="aff" rid="aff1">3</xref></contrib><contrib contrib-type="author"><name><surname>Perlman</surname><given-names>Stanley</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff1">2</xref><xref ref-type="corresp" rid="cor1">*</xref></contrib></contrib-group><aff id="aff1">Departments of Pediatrics,<label>1</label> Microbiology,<label>2</label> Internal Medicine, University of Iowa, Iowa City, Iowa 52242,<label>4</label> Department of Microbiology and Immunology, Loyola University Medical Center, Maywood, Illinois 60153<label>3</label></aff><author-notes><fn id="cor1"><label>*</label><p>Corresponding author. Mailing address: Department of Pediatrics, University of Iowa, Medical Laboratories 2042, Iowa City, IA 52242. Phone: (319) 335-8549. Fax: (319) 335-8991. E-mail: <email>Stanley-Perlman@uiowa.edu</email>.</p></fn><fn id="fn1"><label>†</label><p>L.P. and H.Z. contributed equally to the work.</p></fn></author-notes><pub-date pub-type="ppub"><month>9</month><year>2005</year></pub-date><volume>79</volume><issue>17</issue><fpage>11335</fpage><lpage>11342</lpage><history><date date-type="received"><day>11</day><month>4</month><year>2005</year></date><date date-type="accepted"><day>8</day><month>6</month><year>2005</year></date></history><copyright-statement>Copyright © 2005, American Society for Microbiology</copyright-statement><copyright-year>2005</copyright-year><abstract><p>Most animal species that can be infected with the severe acute respiratory syndrome-associated coronavirus (SARS-CoV) do not reproducibly develop clinical disease, hindering studies of pathogenesis. To develop an alternative system for the study of SARS-CoV, we introduced individual SARS-CoV genes (open reading frames [ORFs]) into the genome of an attenuated murine coronavirus. One protein, the product of SARS-CoV ORF6, converted a sublethal infection to a uniformly lethal encephalitis and enhanced virus growth in tissue culture cells, indicating that SARS-CoV proteins function in the context of a heterologous coronavirus infection. Furthermore, these results suggest that the attenuated murine coronavirus lacks a virulence gene residing in SARS-CoV. Recombinant murine coronaviruses cause a reproducible and well-characterized clinical disease, offer virtually no risk to laboratory personnel, and should be useful for elucidating the role of SARS-CoV nonstructural proteins in viral replication and pathogenesis.</p></abstract><custom-meta-wrap><custom-meta><meta-name>PDF filename</meta-name><meta-value>zjv01705011335</meta-value></custom-meta></custom-meta-wrap></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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