The Immunobiology of SARS*.
Identifieur interne : 003581 ( Main/Exploration ); précédent : 003580; suivant : 003582The Immunobiology of SARS*.
Auteurs : Jun Chen [États-Unis] ; Kanta SubbaraoSource :
- Annual review of immunology [ 0732-0582 ] ; 2007.
Descripteurs français
- KwdFr :
- Animaux, Anticorps antiviraux (immunologie), Chimiokines (immunologie), Humains, Inflammation (immunologie), Interféron de type I (immunologie), Lectines de type C (immunologie), Modèles animaux de maladie humaine, Molécules d'adhérence cellulaire (immunologie), Peptidyl-Dipeptidase A (immunologie), Récepteurs de surface cellulaire (immunologie), Spécificité d'organe, Syndrome respiratoire aigu sévère (immunologie), Virus du SRAS (immunologie).
- MESH :
- immunologie : Anticorps antiviraux, Chimiokines, Inflammation, Interféron de type I, Lectines de type C, Molécules d'adhérence cellulaire, Peptidyl-Dipeptidase A, Récepteurs de surface cellulaire, Syndrome respiratoire aigu sévère, Virus du SRAS.
- Animaux, Humains, Modèles animaux de maladie humaine, Spécificité d'organe.
English descriptors
- KwdEn :
- Animals, Antibodies, Viral (immunology), Cell Adhesion Molecules (immunology), Chemokines (immunology), Disease Models, Animal, Humans, Inflammation (immunology), Interferon Type I (immunology), Lectins, C-Type (immunology), Organ Specificity, Peptidyl-Dipeptidase A (immunology), Receptors, Cell Surface (immunology), SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology).
- MESH :
- chemical , immunology : Antibodies, Viral, Cell Adhesion Molecules, Chemokines, Interferon Type I, Lectins, C-Type, Peptidyl-Dipeptidase A, Receptors, Cell Surface.
- immunology : Inflammation, SARS Virus, Severe Acute Respiratory Syndrome.
- Animals, Disease Models, Animal, Humans, Organ Specificity.
Abstract
Severe acute respiratory syndrome (SARS) presented as an atypical pneumonia that progressed to acute respiratory distress syndrome in approximately 20% of cases and was associated with a mortality of about 10%. The etiological agent was a novel coronavirus (CoV). Angiotensin-converting enzyme 2 is the functional receptor for SARS-CoV; DC-SIGN and CD209L (L-SIGN) can enhance viral entry. Although the virus infects the lungs, gastrointestinal tract, liver, and kidneys, the disease is limited to the lungs, where diffuse alveolar damage is accompanied by a disproportionately sparse inflammatory infiltrate. Pro-inflammatory cytokines and chemokines, particularly IP-10, IL-8, and MCP-1, are elevated in the lungs and peripheral blood, but there is an unusual lack of an antiviral interferon (IFN) response. The virus is susceptible to exogenous type I IFN but suppresses the induction of IFN. Innate immunity is important for viral clearance in the mouse model. Virus-specific neutralizing antibodies that develop during convalescence prevent reinfection in animal models.
DOI: 10.1146/annurev.immunol.25.022106.141706
PubMed: 17243893
Affiliations:
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first="Jun" last="Chen">Jun Chen</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Infectious Diseases, NIAID, NIH, Bethesda, Maryland 20892, USA. chenju@niaid.nih.gov</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, NIAID, NIH, Bethesda, Maryland 20892</wicri:regionArea><wicri:noRegion>Maryland 20892</wicri:noRegion></affiliation></author><author><name sortKey="Subbarao, Kanta" sort="Subbarao, Kanta" uniqKey="Subbarao K" first="Kanta" last="Subbarao">Kanta Subbarao</name></author></analytic><series><title level="j">Annual review of immunology</title><idno type="ISSN">0732-0582</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antibodies, Viral (immunology)</term><term>Cell Adhesion Molecules (immunology)</term><term>Chemokines (immunology)</term><term>Disease Models, Animal</term><term>Humans</term><term>Inflammation (immunology)</term><term>Interferon Type I (immunology)</term><term>Lectins, C-Type (immunology)</term><term>Organ Specificity</term><term>Peptidyl-Dipeptidase A (immunology)</term><term>Receptors, Cell Surface (immunology)</term><term>SARS Virus (immunology)</term><term>Severe Acute Respiratory Syndrome (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Anticorps antiviraux (immunologie)</term><term>Chimiokines (immunologie)</term><term>Humains</term><term>Inflammation (immunologie)</term><term>Interféron de type I (immunologie)</term><term>Lectines de type C (immunologie)</term><term>Modèles animaux de maladie humaine</term><term>Molécules d'adhérence cellulaire (immunologie)</term><term>Peptidyl-Dipeptidase A (immunologie)</term><term>Récepteurs de surface cellulaire (immunologie)</term><term>Spécificité d'organe</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antibodies, Viral</term><term>Cell Adhesion Molecules</term><term>Chemokines</term><term>Interferon Type I</term><term>Lectins, C-Type</term><term>Peptidyl-Dipeptidase A</term><term>Receptors, Cell Surface</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Anticorps antiviraux</term><term>Chimiokines</term><term>Inflammation</term><term>Interféron de type I</term><term>Lectines de type C</term><term>Molécules d'adhérence cellulaire</term><term>Peptidyl-Dipeptidase A</term><term>Récepteurs de surface cellulaire</term><term>Syndrome respiratoire aigu sévère</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Inflammation</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Organ Specificity</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Modèles animaux de maladie humaine</term><term>Spécificité d'organe</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) presented as an atypical pneumonia that progressed to acute respiratory distress syndrome in approximately 20% of cases and was associated with a mortality of about 10%. The etiological agent was a novel coronavirus (CoV). Angiotensin-converting enzyme 2 is the functional receptor for SARS-CoV; DC-SIGN and CD209L (L-SIGN) can enhance viral entry. Although the virus infects the lungs, gastrointestinal tract, liver, and kidneys, the disease is limited to the lungs, where diffuse alveolar damage is accompanied by a disproportionately sparse inflammatory infiltrate. Pro-inflammatory cytokines and chemokines, particularly IP-10, IL-8, and MCP-1, are elevated in the lungs and peripheral blood, but there is an unusual lack of an antiviral interferon (IFN) response. The virus is susceptible to exogenous type I IFN but suppresses the induction of IFN. Innate immunity is important for viral clearance in the mouse model. Virus-specific neutralizing antibodies that develop during convalescence prevent reinfection in animal models.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Subbarao, Kanta" sort="Subbarao, Kanta" uniqKey="Subbarao K" first="Kanta" last="Subbarao">Kanta Subbarao</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Chen, Jun" sort="Chen, Jun" uniqKey="Chen J" first="Jun" last="Chen">Jun Chen</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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