Lethal Infection of K18-hACE2 Mice Infected with Severe Acute Respiratory Syndrome Coronavirus▿
Identifieur interne : 000707 ( Pmc/Curation ); précédent : 000706; suivant : 000708Lethal Infection of K18-hACE2 Mice Infected with Severe Acute Respiratory Syndrome Coronavirus▿
Auteurs : Paul B. Mccray ; Lecia Pewe ; Christine Wohlford-Lenane ; Melissa Hickey ; Lori Manzel ; Lei Shi ; Jason Netland ; Hong Peng Jia ; Carmen Halabi ; Curt D. Sigmund ; David K. Meyerholz ; Patricia Kirby ; Dwight C. Look ; Stanley PerlmanSource :
- Journal of Virology [ 0022-538X ] ; 2006.
Abstract
The severe acute respiratory syndrome (SARS), caused by a novel coronavirus (SARS-CoV), resulted in substantial morbidity, mortality, and economic losses during the 2003 epidemic. While SARS-CoV infection has not recurred to a significant extent since 2003, it still remains a potential threat. Understanding of SARS and development of therapeutic approaches have been hampered by the absence of an animal model that mimics the human disease and is reproducible. Here we show that transgenic mice that express the SARS-CoV receptor (human angiotensin-converting enzyme 2 [hACE2]) in airway and other epithelia develop a rapidly lethal infection after intranasal inoculation with a human strain of the virus. Infection begins in airway epithelia, with subsequent alveolar involvement and extrapulmonary virus spread to the brain. Infection results in macrophage and lymphocyte infiltration in the lungs and upregulation of proinflammatory cytokines and chemokines in both the lung and the brain. This model of lethal infection with SARS-CoV should be useful for studies of pathogenesis and for the development of antiviral therapies.
Url:
DOI: 10.1128/JVI.02012-06
PubMed: 17079315
PubMed Central: 1797474
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Mccray</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Pewe, Lecia" sort="Pewe, Lecia" uniqKey="Pewe L" first="Lecia" last="Pewe">Lecia Pewe</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Wohlford Lenane, Christine" sort="Wohlford Lenane, Christine" uniqKey="Wohlford Lenane C" first="Christine" last="Wohlford-Lenane">Christine Wohlford-Lenane</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Hickey, Melissa" sort="Hickey, Melissa" uniqKey="Hickey M" first="Melissa" last="Hickey">Melissa Hickey</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Manzel, Lori" sort="Manzel, Lori" uniqKey="Manzel L" first="Lori" last="Manzel">Lori Manzel</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="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="Jia, Hong Peng" sort="Jia, Hong Peng" uniqKey="Jia H" first="Hong Peng" last="Jia">Hong Peng Jia</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Halabi, Carmen" sort="Halabi, Carmen" uniqKey="Halabi C" first="Carmen" last="Halabi">Carmen Halabi</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Sigmund, Curt D" sort="Sigmund, Curt D" uniqKey="Sigmund C" first="Curt D." last="Sigmund">Curt D. 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While SARS-CoV infection has not recurred to a significant extent since 2003, it still remains a potential threat. Understanding of SARS and development of therapeutic approaches have been hampered by the absence of an animal model that mimics the human disease and is reproducible. Here we show that transgenic mice that express the SARS-CoV receptor (human angiotensin-converting enzyme 2 [hACE2]) in airway and other epithelia develop a rapidly lethal infection after intranasal inoculation with a human strain of the virus. Infection begins in airway epithelia, with subsequent alveolar involvement and extrapulmonary virus spread to the brain. Infection results in macrophage and lymphocyte infiltration in the lungs and upregulation of proinflammatory cytokines and chemokines in both the lung and the brain. This model of lethal infection with SARS-CoV should be useful for studies of pathogenesis and for the development of antiviral therapies.</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">17079315</article-id><article-id pub-id-type="pmc">1797474</article-id><article-id pub-id-type="publisher-id">2012-06</article-id><article-id pub-id-type="doi">10.1128/JVI.02012-06</article-id><article-categories><subj-group subj-group-type="heading"><subject>Pathogenesis and Immunity</subject></subj-group></article-categories><title-group><article-title>Lethal Infection of K18-<italic>hACE2</italic> Mice Infected with Severe Acute Respiratory Syndrome Coronavirus<xref ref-type="fn" rid="fn1">▿</xref> </article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>McCray</surname><given-names>Paul B.</given-names><suffix>Jr.</suffix></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff1">6</xref><xref ref-type="corresp" rid="cor1">*</xref></contrib><contrib contrib-type="author"><name><surname>Pewe</surname><given-names>Lecia</given-names></name><xref ref-type="aff" rid="aff1">2</xref></contrib><contrib contrib-type="author"><name><surname>Wohlford-Lenane</surname><given-names>Christine</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Hickey</surname><given-names>Melissa</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Manzel</surname><given-names>Lori</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">3</xref></contrib><contrib contrib-type="author"><name><surname>Netland</surname><given-names>Jason</given-names></name><xref ref-type="aff" rid="aff1">5</xref></contrib><contrib contrib-type="author"><name><surname>Jia</surname><given-names>Hong Peng</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Halabi</surname><given-names>Carmen</given-names></name><xref ref-type="aff" rid="aff1">2</xref><xref ref-type="aff" rid="aff1">6</xref></contrib><contrib contrib-type="author"><name><surname>Sigmund</surname><given-names>Curt D.</given-names></name><xref ref-type="aff" rid="aff1">2</xref><xref ref-type="aff" rid="aff1">6</xref></contrib><contrib contrib-type="author"><name><surname>Meyerholz</surname><given-names>David K.</given-names></name><xref ref-type="aff" rid="aff1">4</xref></contrib><contrib contrib-type="author"><name><surname>Kirby</surname><given-names>Patricia</given-names></name><xref ref-type="aff" rid="aff1">4</xref></contrib><contrib contrib-type="author"><name><surname>Look</surname><given-names>Dwight C.</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="aff" rid="aff1">5</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,<label>3</label> Pathology,<label>4</label> Interdisciplinary Programs in Immunology,<label>5</label> Genetics, University of Iowa, Iowa City, Iowa 52242<label>6</label></aff><author-notes><fn id="cor1"><label>*</label><p>Corresponding author. Mailing address for Paul B. McCray, Jr.: Department of Pediatrics, University of Iowa, Iowa City, IA 52242. Phone: (319) 335-6844. Fax: (319) 335-6925. E-mail: <email>Paul-McCray@uiowa.edu</email>. Mailing address for Stanley Perlman: Department of Microbiology, University of Iowa, Iowa City, IA 52242. Phone: (319) 335-8549. Fax: (319) 335-9999. E-mail: <email>stanley-perlman@uiowa.edu</email>.</p></fn></author-notes><pub-date pub-type="ppub"><month>1</month><year>2007</year></pub-date><pub-date pub-type="epub"><day>1</day><month>11</month><year>2006</year></pub-date><volume>81</volume><issue>2</issue><fpage>813</fpage><lpage>821</lpage><history><date date-type="received"><day>24</day><month>9</month><year>2006</year></date><date date-type="accepted"><day>20</day><month>10</month><year>2006</year></date></history><copyright-statement>Copyright © 2007, American Society for Microbiology</copyright-statement><copyright-year>2007</copyright-year><self-uri xlink:title="pdf" xlink:href="zjv00207000813.pdf"></self-uri><abstract><p>The severe acute respiratory syndrome (SARS), caused by a novel coronavirus (SARS-CoV), resulted in substantial morbidity, mortality, and economic losses during the 2003 epidemic. While SARS-CoV infection has not recurred to a significant extent since 2003, it still remains a potential threat. Understanding of SARS and development of therapeutic approaches have been hampered by the absence of an animal model that mimics the human disease and is reproducible. Here we show that transgenic mice that express the SARS-CoV receptor (human angiotensin-converting enzyme 2 [hACE2]) in airway and other epithelia develop a rapidly lethal infection after intranasal inoculation with a human strain of the virus. Infection begins in airway epithelia, with subsequent alveolar involvement and extrapulmonary virus spread to the brain. Infection results in macrophage and lymphocyte infiltration in the lungs and upregulation of proinflammatory cytokines and chemokines in both the lung and the brain. This model of lethal infection with SARS-CoV should be useful for studies of pathogenesis and for the development of antiviral therapies.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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