SrasV1, PascalFrancis, Curation, bibRecord, 000605

Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus

Identifieur interne : 000605 ( PascalFrancis/Curation ); précédent : 000604; suivant : 000606

Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus

Auteurs : Paul B. Jr Mccray [États-Unis] ; Lecia Pewe [États-Unis] ; Christine Wohlford-Lenane [États-Unis] ; Melissa Hickey [États-Unis] ; Lori Manzel [États-Unis] ; LEI SHI [États-Unis] ; Jason Netland [États-Unis] ; HONG PENG JIA [États-Unis] ; Carmen Halabi [États-Unis] ; Curt D. Sigmund [États-Unis] ; David K. Meyerholz [États-Unis] ; Patricia Kirby [États-Unis] ; Dwight C. Look [États-Unis] ; Stanley Perlman [États-Unis]

Source :

Journal of virology [ 0022-538X ] ; 2007.

RBID : Pascal:07-0182099

Descripteurs français

Pascal (Inist)
- Souris, Coronavirus, Virologie, Infection, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Coronavirus, Infection, Mouse, Severe acute respiratory syndrome, Virology.

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.

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A03		`1`		`@0 J. virol.`
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A08	`01`	`1`	`ENG`	`@1 Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus`
A11	`01`	`1`		`@1 MCCRAY (Paul B. JR)`
A11	`02`	`1`		`@1 PEWE (Lecia)`
A11	`03`	`1`		`@1 WOHLFORD-LENANE (Christine)`
A11	`04`	`1`		`@1 HICKEY (Melissa)`
A11	`05`	`1`		`@1 MANZEL (Lori)`
A11	`06`	`1`		`@1 LEI SHI`
A11	`07`	`1`		`@1 NETLAND (Jason)`
A11	`08`	`1`		`@1 HONG PENG JIA`
A11	`09`	`1`		`@1 HALABI (Carmen)`
A11	`10`	`1`		`@1 SIGMUND (Curt D.)`
A11	`11`	`1`		`@1 MEYERHOLZ (David K.)`
A11	`12`	`1`		`@1 KIRBY (Patricia)`
A11	`13`	`1`		`@1 LOOK (Dwight C.)`
A11	`14`	`1`		`@1 PERLMAN (Stanley)`
A14	`01`			`@1 Department of Pediatrics, University of Iowa @2 Iowa City, Iowa 52242 @3 USA @Z 1 aut. @Z 3 aut. @Z 4 aut. @Z 8 aut. @Z 14 aut.`
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A14	`03`			`@1 Department of Microbiology, University of Iowa @2 Iowa City, Iowa 52242 @3 USA @Z 2 aut. @Z 9 aut. @Z 10 aut. @Z 14 aut.`
A14	`04`			`@1 Department of Internal Medicine, University of Iowa @2 Iowa City, Iowa 52242 @3 USA @Z 5 aut. @Z 6 aut. @Z 13 aut.`
A14	`05`			`@1 Department of Interdisciplinary Programs in Immunology, University of Iowa @2 Iowa City, Iowa 52242 @3 USA @Z 7 aut. @Z 14 aut.`
A14	`06`			`@1 Department of Pathology, University of Iowa @2 Iowa City, Iowa 52242 @3 USA @Z 11 aut. @Z 12 aut.`
A20				`@1 813-821`
A21				`@1 2007`
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A64	`01`	`1`		`@0 Journal of virology`
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C01	`01`		`ENG`	@0 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.
C02	`01`	`X`		`@0 002A05C10`
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C03	`02`	`X`	`FRE`	`@0 Coronavirus @2 NW @5 02`
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C03	`02`	`X`	`SPA`	`@0 Coronavirus @2 NW @5 02`
C03	`03`	`X`	`FRE`	`@0 Virologie @5 05`
C03	`03`	`X`	`ENG`	`@0 Virology @5 05`
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C03	`04`	`X`	`FRE`	`@0 Infection @5 14`
C03	`04`	`X`	`ENG`	`@0 Infection @5 14`
C03	`04`	`X`	`SPA`	`@0 Infección @5 14`
C03	`05`	`X`	`FRE`	`@0 Syndrome respiratoire aigu sévère @2 NM @5 15`
C03	`05`	`X`	`ENG`	`@0 Severe acute respiratory syndrome @2 NM @5 15`
C03	`05`	`X`	`SPA`	`@0 Síndrome respiratorio agudo severo @2 NM @5 15`
C07	`01`	`X`	`FRE`	`@0 Rodentia @2 NS`
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C07	`02`	`X`	`FRE`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`ENG`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`SPA`	`@0 Mammalia @2 NS`
C07	`03`	`X`	`FRE`	`@0 Vertebrata @2 NS`
C07	`03`	`X`	`ENG`	`@0 Vertebrata @2 NS`
C07	`03`	`X`	`SPA`	`@0 Vertebrata @2 NS`
C07	`04`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`04`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
C07	`04`	`X`	`SPA`	`@0 Coronaviridae @2 NW`
C07	`05`	`X`	`FRE`	`@0 Nidovirales @2 NW`
C07	`05`	`X`	`ENG`	`@0 Nidovirales @2 NW`
C07	`05`	`X`	`SPA`	`@0 Nidovirales @2 NW`
C07	`06`	`X`	`FRE`	`@0 Virus @2 NW`
C07	`06`	`X`	`ENG`	`@0 Virus @2 NW`
C07	`06`	`X`	`SPA`	`@0 Virus @2 NW`
C07	`07`	`X`	`FRE`	`@0 Appareil respiratoire pathologie @5 13`
C07	`07`	`X`	`ENG`	`@0 Respiratory disease @5 13`
C07	`07`	`X`	`SPA`	`@0 Aparato respiratorio patología @5 13`
C07	`08`	`X`	`FRE`	`@0 Virose`
C07	`08`	`X`	`ENG`	`@0 Viral disease`
C07	`08`	`X`	`SPA`	`@0 Virosis`
C07	`09`	`X`	`FRE`	`@0 Poumon pathologie @5 16`
C07	`09`	`X`	`ENG`	`@0 Lung disease @5 16`
C07	`09`	`X`	`SPA`	`@0 Pulmón patología @5 16`
N21				`@1 122`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

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Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus</title>
<author><name sortKey="Mccray, Paul B Jr" sort="Mccray, Paul B Jr" uniqKey="Mccray P" first="Paul B. Jr" last="Mccray">Paul B. Jr Mccray</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Pediatrics, University of Iowa</s1>
<s2>Iowa City, Iowa 52242</s2>
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<country>États-Unis</country>
</affiliation>
<affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Genetics, University of Iowa</s1>
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<author><name sortKey="Pewe, Lecia" sort="Pewe, Lecia" uniqKey="Pewe L" first="Lecia" last="Pewe">Lecia Pewe</name>
<affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Microbiology, University of Iowa</s1>
<s2>Iowa City, Iowa 52242</s2>
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</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 wicri:level="1"><inist:fA14 i1="01"><s1>Department of Pediatrics, University of Iowa</s1>
<s2>Iowa City, Iowa 52242</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
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<sZ>4 aut.</sZ>
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<country>États-Unis</country>
</affiliation>
</author>
<author><name sortKey="Hickey, Melissa" sort="Hickey, Melissa" uniqKey="Hickey M" first="Melissa" last="Hickey">Melissa Hickey</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Pediatrics, University of Iowa</s1>
<s2>Iowa City, Iowa 52242</s2>
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<author><name sortKey="Manzel, Lori" sort="Manzel, Lori" uniqKey="Manzel L" first="Lori" last="Manzel">Lori Manzel</name>
<affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Internal Medicine, University of Iowa</s1>
<s2>Iowa City, Iowa 52242</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
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<country>États-Unis</country>
</affiliation>
</author>
<author><name sortKey="Lei Shi" sort="Lei Shi" uniqKey="Lei Shi" last="Lei Shi">LEI SHI</name>
<affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Internal Medicine, University of Iowa</s1>
<s2>Iowa City, Iowa 52242</s2>
<s3>USA</s3>
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<country>États-Unis</country>
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<series><title level="j" type="main">Journal of virology</title>
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<idno type="ISSN">0022-538X</idno>
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<front><div type="abstract" xml:lang="en">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.</div>
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<fA08 i1="01" i2="1" l="ENG"><s1>Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus</s1>
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Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus

Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus

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