Resolution of primary severe acute respiratory syndrome-associated coronavirus infection requires Stat1.
Identifieur interne : 000A92 ( Ncbi/Curation ); précédent : 000A91; suivant : 000A93Resolution of primary severe acute respiratory syndrome-associated coronavirus infection requires Stat1.
Auteurs : Robert J. Hogan [États-Unis] ; Guangping Gao ; Thomas Rowe ; Peter Bell ; Douglas Flieder ; Jason Paragas ; Gary P. Kobinger ; Nelson A. Wivel ; Ronald G. Crystal ; Julie Boyer ; Heinz Feldmann ; Thomas G. Voss ; James M. WilsonSource :
- Journal of virology [ 0022-538X ] ; 2004.
Descripteurs français
- KwdFr :
- Animaux, Bronchiolite virale (virologie), Facteur de transcription STAT-1, Immunohistochimie, Poumon (anatomopathologie), Poumon (virologie), Protéines de liaison à l'ADN (génétique), Protéines de liaison à l'ADN (métabolisme), Souris, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (physiopathologie), Syndrome respiratoire aigu sévère (virologie), Transactivateurs (génétique), Transactivateurs (métabolisme), Virus du SRAS (pathogénicité).
- MESH :
- anatomopathologie : Poumon, Syndrome respiratoire aigu sévère.
- génétique : Protéines de liaison à l'ADN, Transactivateurs.
- immunologie : Syndrome respiratoire aigu sévère.
- métabolisme : Protéines de liaison à l'ADN, Transactivateurs.
- pathogénicité : Virus du SRAS.
- physiopathologie : Syndrome respiratoire aigu sévère.
- virologie : Bronchiolite virale, Poumon, Syndrome respiratoire aigu sévère.
- Animaux, Facteur de transcription STAT-1, Immunohistochimie, Souris.
English descriptors
- KwdEn :
- Animals, Bronchiolitis, Viral (virology), DNA-Binding Proteins (genetics), DNA-Binding Proteins (metabolism), Immunohistochemistry, Lung (pathology), Lung (virology), Mice, SARS Virus (pathogenicity), STAT1 Transcription Factor, Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (physiopathology), Severe Acute Respiratory Syndrome (virology), Trans-Activators (genetics), Trans-Activators (metabolism).
- MESH :
- chemical , genetics : DNA-Binding Proteins, Trans-Activators.
- chemical , metabolism : DNA-Binding Proteins, Trans-Activators.
- immunology : Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- pathology : Lung, Severe Acute Respiratory Syndrome.
- physiopathology : Severe Acute Respiratory Syndrome.
- virology : Bronchiolitis, Viral, Lung, Severe Acute Respiratory Syndrome.
- Animals, Immunohistochemistry, Mice, STAT1 Transcription Factor.
Abstract
Intranasal inhalation of the severe acute respiratory syndrome coronavirus (SARS CoV) in the immunocompetent mouse strain 129SvEv resulted in infection of conducting airway epithelial cells followed by rapid clearance of virus from the lungs and the development of self-limited bronchiolitis. Animals resistant to the effects of interferons by virtue of a deficiency in Stat1 demonstrated a markedly different course following intranasal inhalation of SARS CoV, one characterized by replication of virus in lungs and progressively worsening pulmonary disease with inflammation of small airways and alveoli and systemic spread of the virus to livers and spleens.
DOI: 10.1128/JVI.78.20.11416-11421.2004
PubMed: 15452265
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pubmed:15452265Le document en format XML
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<term>Bronchiolitis, Viral (virology)</term>
<term>DNA-Binding Proteins (genetics)</term>
<term>DNA-Binding Proteins (metabolism)</term>
<term>Immunohistochemistry</term>
<term>Lung (pathology)</term>
<term>Lung (virology)</term>
<term>Mice</term>
<term>SARS Virus (pathogenicity)</term>
<term>STAT1 Transcription Factor</term>
<term>Severe Acute Respiratory Syndrome (immunology)</term>
<term>Severe Acute Respiratory Syndrome (pathology)</term>
<term>Severe Acute Respiratory Syndrome (physiopathology)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Trans-Activators (genetics)</term>
<term>Trans-Activators (metabolism)</term>
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<term>Bronchiolite virale (virologie)</term>
<term>Facteur de transcription STAT-1</term>
<term>Immunohistochimie</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (virologie)</term>
<term>Protéines de liaison à l'ADN (génétique)</term>
<term>Protéines de liaison à l'ADN (métabolisme)</term>
<term>Souris</term>
<term>Syndrome respiratoire aigu sévère (anatomopathologie)</term>
<term>Syndrome respiratoire aigu sévère (immunologie)</term>
<term>Syndrome respiratoire aigu sévère (physiopathologie)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Transactivateurs (génétique)</term>
<term>Transactivateurs (métabolisme)</term>
<term>Virus du SRAS (pathogénicité)</term>
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<term>Trans-Activators</term>
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<term>Trans-Activators</term>
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<term>Syndrome respiratoire aigu sévère</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines de liaison à l'ADN</term>
<term>Transactivateurs</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines de liaison à l'ADN</term>
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<term>Severe Acute Respiratory Syndrome</term>
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<term>Poumon</term>
<term>Syndrome respiratoire aigu sévère</term>
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<term>Lung</term>
<term>Severe Acute Respiratory Syndrome</term>
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<term>Immunohistochemistry</term>
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<front><div type="abstract" xml:lang="en">Intranasal inhalation of the severe acute respiratory syndrome coronavirus (SARS CoV) in the immunocompetent mouse strain 129SvEv resulted in infection of conducting airway epithelial cells followed by rapid clearance of virus from the lungs and the development of self-limited bronchiolitis. Animals resistant to the effects of interferons by virtue of a deficiency in Stat1 demonstrated a markedly different course following intranasal inhalation of SARS CoV, one characterized by replication of virus in lungs and progressively worsening pulmonary disease with inflammation of small airways and alveoli and systemic spread of the virus to livers and spleens.</div>
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