Mechanisms of host defense following severe acute respiratory syndrome-coronavirus (SARS-CoV) pulmonary infection of mice.
Identifieur interne : 005250 ( Main/Exploration ); précédent : 005249; suivant : 005251Mechanisms of host defense following severe acute respiratory syndrome-coronavirus (SARS-CoV) pulmonary infection of mice.
Auteurs : William G. Glass [États-Unis] ; Kanta Subbarao ; Brian Murphy ; Philip M. MurphySource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 2004.
Descripteurs français
- KwdFr :
- Administration par voie nasale, Animaux, Cellules tueuses naturelles (immunologie), Cellules tueuses naturelles (virologie), Charge virale, Chimiokines (biosynthèse), Encéphale (immunologie), Encéphale (virologie), Femelle, Immunité innée, Lymphocytes B (immunologie), Lymphocytes B (virologie), Lymphocytes T (immunologie), Lymphocytes T (virologie), Médiateurs de l'inflammation (métabolisme), Poumon (anatomopathologie), Poumon (immunologie), Poumon (virologie), Retard de croissance staturo-pondérale (anatomopathologie), Retard de croissance staturo-pondérale (immunologie), Retard de croissance staturo-pondérale (virologie), Régulation positive (immunologie), Réplication virale (immunologie), Souris, Souris de lignée C57BL, Souris knockout, Sous-populations de lymphocytes T (immunologie), Sous-populations de lymphocytes T (virologie), Spécificité d'organe (immunologie), Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (physiopathologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (immunologie), Virus du SRAS (isolement et purification).
- MESH :
- anatomopathologie : Poumon, Retard de croissance staturo-pondérale, Syndrome respiratoire aigu sévère.
- biosynthèse : Chimiokines.
- immunologie : Cellules tueuses naturelles, Encéphale, Lymphocytes B, Lymphocytes T, Poumon, Retard de croissance staturo-pondérale, Régulation positive, Réplication virale, Sous-populations de lymphocytes T, Spécificité d'organe, Syndrome respiratoire aigu sévère, Virus du SRAS.
- isolement et purification : Virus du SRAS.
- métabolisme : Médiateurs de l'inflammation.
- physiopathologie : Syndrome respiratoire aigu sévère.
- virologie : Cellules tueuses naturelles, Encéphale, Lymphocytes B, Lymphocytes T, Poumon, Retard de croissance staturo-pondérale, Sous-populations de lymphocytes T, Syndrome respiratoire aigu sévère.
- Administration par voie nasale, Animaux, Charge virale, Femelle, Immunité innée, Souris, Souris de lignée C57BL, Souris knockout.
English descriptors
- KwdEn :
- Administration, Intranasal, Animals, B-Lymphocytes (immunology), B-Lymphocytes (virology), Brain (immunology), Brain (virology), Chemokines (biosynthesis), Failure to Thrive (immunology), Failure to Thrive (pathology), Failure to Thrive (virology), Female, Immunity, Innate, Inflammation Mediators (metabolism), Killer Cells, Natural (immunology), Killer Cells, Natural (virology), Lung (immunology), Lung (pathology), Lung (virology), Mice, Mice, Inbred C57BL, Mice, Knockout, Organ Specificity (immunology), SARS Virus (immunology), SARS Virus (isolation & purification), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (physiopathology), Severe Acute Respiratory Syndrome (virology), T-Lymphocyte Subsets (immunology), T-Lymphocyte Subsets (virology), T-Lymphocytes (immunology), T-Lymphocytes (virology), Up-Regulation (immunology), Viral Load, Virus Replication (immunology).
- MESH :
- chemical , biosynthesis : Chemokines.
- immunology : B-Lymphocytes, Brain, Failure to Thrive, Killer Cells, Natural, Lung, Organ Specificity, SARS Virus, Severe Acute Respiratory Syndrome, T-Lymphocyte Subsets, T-Lymphocytes, Up-Regulation, Virus Replication.
- isolation & purification : SARS Virus.
- chemical , metabolism : Inflammation Mediators.
- pathology : Failure to Thrive, Lung, Severe Acute Respiratory Syndrome.
- physiopathology : Severe Acute Respiratory Syndrome.
- virology : B-Lymphocytes, Brain, Failure to Thrive, Killer Cells, Natural, Lung, Severe Acute Respiratory Syndrome, T-Lymphocyte Subsets, T-Lymphocytes.
- Administration, Intranasal, Animals, Female, Immunity, Innate, Mice, Mice, Inbred C57BL, Mice, Knockout, Viral Load.
Abstract
We describe a model of severe acute respiratory syndrome-coronavirus (SARS-CoV) infection in C57BL/6 mice. A clinical isolate of the virus introduced intranasally replicated transiently to high levels in the lungs of these mice, with a peak on day 3 and clearance by day 9 postinfection. Viral RNA localized to bronchial and bronchiolar epithelium. Expression of mRNA for angiotensin converting enzyme 2, the SARS-CoV receptor, was detected in the lung following infection. The virus induced production in the lung of the proinflammatory chemokines CCL2, CCL3, CCL5, CXCL9, and CXCL10 with differential kinetics. The receptors for these chemokines were also detected. Most impressively, mRNA for CXCR3, the receptor for CXCL9 and CXCL10, was massively up-regulated in the lungs of SARS-CoV-infected mice. Surprisingly Th1 (and Th2) cytokines were not detectable, and there was little local accumulation of leukocytes and no obvious clinical signs of pulmonary dysfunction. Moreover, beige, CD1-/-, and RAG1-/- mice cleared the virus normally. Infection spread to the brain as it was cleared from the lung, again without leukocyte accumulation. Infected mice had a relative failure to thrive, gaining weight significantly more slowly than uninfected mice. These data indicate that C57BL/6 mice support transient nonfatal systemic infection with SARS-CoV in the lung, which is able to disseminate to brain. In this species, proinflammatory chemokines may coordinate a rapid and highly effective innate antiviral response in the lung, but NK cells and adaptive cellular immunity are not required for viral clearance.
DOI: 10.4049/jimmunol.173.6.4030
PubMed: 15356152
Affiliations:
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Le document en format XML
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<author><name sortKey="Glass, William G" sort="Glass, William G" uniqKey="Glass W" first="William G" last="Glass">William G. Glass</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea>
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<author><name sortKey="Subbarao, Kanta" sort="Subbarao, Kanta" uniqKey="Subbarao K" first="Kanta" last="Subbarao">Kanta Subbarao</name>
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<author><name sortKey="Murphy, Brian" sort="Murphy, Brian" uniqKey="Murphy B" first="Brian" last="Murphy">Brian Murphy</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Mechanisms of host defense following severe acute respiratory syndrome-coronavirus (SARS-CoV) pulmonary infection of mice.</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Administration, Intranasal</term>
<term>Animals</term>
<term>B-Lymphocytes (immunology)</term>
<term>B-Lymphocytes (virology)</term>
<term>Brain (immunology)</term>
<term>Brain (virology)</term>
<term>Chemokines (biosynthesis)</term>
<term>Failure to Thrive (immunology)</term>
<term>Failure to Thrive (pathology)</term>
<term>Failure to Thrive (virology)</term>
<term>Female</term>
<term>Immunity, Innate</term>
<term>Inflammation Mediators (metabolism)</term>
<term>Killer Cells, Natural (immunology)</term>
<term>Killer Cells, Natural (virology)</term>
<term>Lung (immunology)</term>
<term>Lung (pathology)</term>
<term>Lung (virology)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Organ Specificity (immunology)</term>
<term>SARS Virus (immunology)</term>
<term>SARS Virus (isolation & purification)</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>T-Lymphocyte Subsets (immunology)</term>
<term>T-Lymphocyte Subsets (virology)</term>
<term>T-Lymphocytes (immunology)</term>
<term>T-Lymphocytes (virology)</term>
<term>Up-Regulation (immunology)</term>
<term>Viral Load</term>
<term>Virus Replication (immunology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Administration par voie nasale</term>
<term>Animaux</term>
<term>Cellules tueuses naturelles (immunologie)</term>
<term>Cellules tueuses naturelles (virologie)</term>
<term>Charge virale</term>
<term>Chimiokines (biosynthèse)</term>
<term>Encéphale (immunologie)</term>
<term>Encéphale (virologie)</term>
<term>Femelle</term>
<term>Immunité innée</term>
<term>Lymphocytes B (immunologie)</term>
<term>Lymphocytes B (virologie)</term>
<term>Lymphocytes T (immunologie)</term>
<term>Lymphocytes T (virologie)</term>
<term>Médiateurs de l'inflammation (métabolisme)</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (immunologie)</term>
<term>Poumon (virologie)</term>
<term>Retard de croissance staturo-pondérale (anatomopathologie)</term>
<term>Retard de croissance staturo-pondérale (immunologie)</term>
<term>Retard de croissance staturo-pondérale (virologie)</term>
<term>Régulation positive (immunologie)</term>
<term>Réplication virale (immunologie)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Sous-populations de lymphocytes T (immunologie)</term>
<term>Sous-populations de lymphocytes T (virologie)</term>
<term>Spécificité d'organe (immunologie)</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>Virus du SRAS (immunologie)</term>
<term>Virus du SRAS (isolement et purification)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Chemokines</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Poumon</term>
<term>Retard de croissance staturo-pondérale</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Chimiokines</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules tueuses naturelles</term>
<term>Encéphale</term>
<term>Lymphocytes B</term>
<term>Lymphocytes T</term>
<term>Poumon</term>
<term>Retard de croissance staturo-pondérale</term>
<term>Régulation positive</term>
<term>Réplication virale</term>
<term>Sous-populations de lymphocytes T</term>
<term>Spécificité d'organe</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>B-Lymphocytes</term>
<term>Brain</term>
<term>Failure to Thrive</term>
<term>Killer Cells, Natural</term>
<term>Lung</term>
<term>Organ Specificity</term>
<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
<term>T-Lymphocyte Subsets</term>
<term>T-Lymphocytes</term>
<term>Up-Regulation</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" qualifier="isolation & purification" xml:lang="en"><term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr"><term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Inflammation Mediators</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Médiateurs de l'inflammation</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Failure to Thrive</term>
<term>Lung</term>
<term>Severe Acute Respiratory Syndrome</term>
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<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
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<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term>
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<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Cellules tueuses naturelles</term>
<term>Encéphale</term>
<term>Lymphocytes B</term>
<term>Lymphocytes T</term>
<term>Poumon</term>
<term>Retard de croissance staturo-pondérale</term>
<term>Sous-populations de lymphocytes T</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>B-Lymphocytes</term>
<term>Brain</term>
<term>Failure to Thrive</term>
<term>Killer Cells, Natural</term>
<term>Lung</term>
<term>Severe Acute Respiratory Syndrome</term>
<term>T-Lymphocyte Subsets</term>
<term>T-Lymphocytes</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Administration, Intranasal</term>
<term>Animals</term>
<term>Female</term>
<term>Immunity, Innate</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Viral Load</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Administration par voie nasale</term>
<term>Animaux</term>
<term>Charge virale</term>
<term>Femelle</term>
<term>Immunité innée</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
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<front><div type="abstract" xml:lang="en">We describe a model of severe acute respiratory syndrome-coronavirus (SARS-CoV) infection in C57BL/6 mice. A clinical isolate of the virus introduced intranasally replicated transiently to high levels in the lungs of these mice, with a peak on day 3 and clearance by day 9 postinfection. Viral RNA localized to bronchial and bronchiolar epithelium. Expression of mRNA for angiotensin converting enzyme 2, the SARS-CoV receptor, was detected in the lung following infection. The virus induced production in the lung of the proinflammatory chemokines CCL2, CCL3, CCL5, CXCL9, and CXCL10 with differential kinetics. The receptors for these chemokines were also detected. Most impressively, mRNA for CXCR3, the receptor for CXCL9 and CXCL10, was massively up-regulated in the lungs of SARS-CoV-infected mice. Surprisingly Th1 (and Th2) cytokines were not detectable, and there was little local accumulation of leukocytes and no obvious clinical signs of pulmonary dysfunction. Moreover, beige, CD1-/-, and RAG1-/- mice cleared the virus normally. Infection spread to the brain as it was cleared from the lung, again without leukocyte accumulation. Infected mice had a relative failure to thrive, gaining weight significantly more slowly than uninfected mice. These data indicate that C57BL/6 mice support transient nonfatal systemic infection with SARS-CoV in the lung, which is able to disseminate to brain. In this species, proinflammatory chemokines may coordinate a rapid and highly effective innate antiviral response in the lung, but NK cells and adaptive cellular immunity are not required for viral clearance.</div>
</front>
</TEI>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Maryland</li>
</region>
</list>
<tree><noCountry><name sortKey="Murphy, Brian" sort="Murphy, Brian" uniqKey="Murphy B" first="Brian" last="Murphy">Brian Murphy</name>
<name sortKey="Murphy, Philip M" sort="Murphy, Philip M" uniqKey="Murphy P" first="Philip M" last="Murphy">Philip M. Murphy</name>
<name sortKey="Subbarao, Kanta" sort="Subbarao, Kanta" uniqKey="Subbarao K" first="Kanta" last="Subbarao">Kanta Subbarao</name>
</noCountry>
<country name="États-Unis"><region name="Maryland"><name sortKey="Glass, William G" sort="Glass, William G" uniqKey="Glass W" first="William G" last="Glass">William G. Glass</name>
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