Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus.
Identifieur interne : 002000 ( PubMed/Curation ); précédent : 001F99; suivant : 002001Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus.
Auteurs : Paul B. Mccray [États-Unis] ; 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 ] ; 2007.
Descripteurs français
- KwdFr :
- Animaux, Cellules épithéliales (anatomopathologie), Cellules épithéliales (virologie), Encéphale (anatomopathologie), Encéphale (cytologie), Encéphale (virologie), Humains, Kératine-18 (génétique), Kératine-18 (métabolisme), Modèles animaux de maladie humaine, Peptidyl-Dipeptidase A (génétique), Peptidyl-Dipeptidase A (métabolisme), Poumon (anatomopathologie), Poumon (cytologie), Poumon (virologie), Souris, Souris de lignée C57BL, Souris transgéniques, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (mortalité), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (pathogénicité).
- MESH :
- anatomopathologie : Cellules épithéliales, Encéphale, Poumon, Syndrome respiratoire aigu sévère.
- cytologie : Encéphale, Poumon.
- génétique : Kératine-18, Peptidyl-Dipeptidase A.
- mortalité : Syndrome respiratoire aigu sévère.
- métabolisme : Kératine-18, Peptidyl-Dipeptidase A.
- pathogénicité : Virus du SRAS.
- virologie : Cellules épithéliales, Encéphale, Poumon, Syndrome respiratoire aigu sévère.
- Animaux, Humains, Modèles animaux de maladie humaine, Souris, Souris de lignée C57BL, Souris transgéniques.
English descriptors
- KwdEn :
- Animals, Brain (cytology), Brain (pathology), Brain (virology), Disease Models, Animal, Epithelial Cells (pathology), Epithelial Cells (virology), Humans, Keratin-18 (genetics), Keratin-18 (metabolism), Lung (cytology), Lung (pathology), Lung (virology), Mice, Mice, Inbred C57BL, Mice, Transgenic, Peptidyl-Dipeptidase A (genetics), Peptidyl-Dipeptidase A (metabolism), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (mortality), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology).
- MESH :
- chemical , genetics : Keratin-18, Peptidyl-Dipeptidase A.
- cytology : Brain, Lung.
- chemical , metabolism : Keratin-18, Peptidyl-Dipeptidase A.
- mortality : Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- pathology : Brain, Epithelial Cells, Lung, Severe Acute Respiratory Syndrome.
- virology : Brain, Epithelial Cells, Lung, Severe Acute Respiratory Syndrome.
- Animals, Disease Models, Animal, Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic.
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.
DOI: 10.1128/JVI.02012-06
PubMed: 17079315
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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>
</front>
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<ArticleTitle>Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus.</ArticleTitle>
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<Abstract><AbstractText>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.</AbstractText>
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