Pathogenesis of severe acute respiratory syndrome
Identifieur interne : 001005 ( Ncbi/Merge ); précédent : 001004; suivant : 001006Pathogenesis of severe acute respiratory syndrome
Auteurs : Yu Lung Lau [Hong Kong] ; Js Malik Peiris [Hong Kong]Source :
- Current Opinion in Immunology [ 0952-7915 ] ; 2005.
Descripteurs français
- KwdFr :
- Animaux, Humains, Immunité innée (immunologie), Poumon (anatomopathologie), Poumon (immunologie), Poumon (virologie), Prédisposition génétique à une maladie, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (immunologie), Virus du SRAS (pathogénicité), Virus du SRAS (physiologie).
- MESH :
- anatomopathologie : Poumon, Syndrome respiratoire aigu sévère.
- génétique : Syndrome respiratoire aigu sévère.
- immunologie : Immunité innée, Poumon, Syndrome respiratoire aigu sévère, Virus du SRAS.
- pathogénicité : Virus du SRAS.
- physiologie : Virus du SRAS.
- virologie : Poumon, Syndrome respiratoire aigu sévère.
- Animaux, Humains, Prédisposition génétique à une maladie.
English descriptors
- KwdEn :
- Animals, Genetic Predisposition to Disease, Humans, Immunity, Innate (immunology), Lung (immunology), Lung (pathology), Lung (virology), SARS Virus (immunology), SARS Virus (pathogenicity), SARS Virus (physiology), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology).
- MESH :
- genetics : Severe Acute Respiratory Syndrome.
- immunology : Immunity, Innate, Lung, SARS Virus, Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- pathology : Lung, Severe Acute Respiratory Syndrome.
- physiology : SARS Virus.
- virology : Lung, Severe Acute Respiratory Syndrome.
- Animals, Genetic Predisposition to Disease, Humans.
Abstract
Severe acute respiratory syndrome (SARS) is a zoonotic infectious disease caused by a novel coronavirus (CoV). The tissue tropism of SARS-CoV includes not only the lung, but also the gastrointestinal tract, kidney and liver. Angiotensin-converting enzyme 2 (ACE2), the C-type lectin CD209L (also known L-SIGN), and DC-SIGN bind SARS-CoV, but ACE2 appears to be the key functional receptor for the virus. There is a prominent innate immune response to SARS-CoV infection, including acute-phase proteins, chemokines, inflammatory cytokines and C-type lectins such as mannose-binding lectin, which plays a protective role against SARS. By contrast there may be a lack of type 1 interferon response. Moreover, lymphopenia with decreased numbers of CD4+ and CD8+ T cells is common during the acute phase. Convalescent patients have IgG-class neutralizing antibodies that recognize amino acids 441–700 of the spike protein (S protein) as the major epitope.
Url:
DOI: 10.1016/j.coi.2005.05.009
PubMed: 15950449
PubMed Central: 7127490
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<term>Immunity, Innate (immunology)</term>
<term>Lung (immunology)</term>
<term>Lung (pathology)</term>
<term>Lung (virology)</term>
<term>SARS Virus (immunology)</term>
<term>SARS Virus (pathogenicity)</term>
<term>SARS Virus (physiology)</term>
<term>Severe Acute Respiratory Syndrome (genetics)</term>
<term>Severe Acute Respiratory Syndrome (immunology)</term>
<term>Severe Acute Respiratory Syndrome (pathology)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
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<term>Humains</term>
<term>Immunité innée (immunologie)</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (immunologie)</term>
<term>Poumon (virologie)</term>
<term>Prédisposition génétique à une maladie</term>
<term>Syndrome respiratoire aigu sévère (anatomopathologie)</term>
<term>Syndrome respiratoire aigu sévère (génétique)</term>
<term>Syndrome respiratoire aigu sévère (immunologie)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Virus du SRAS (immunologie)</term>
<term>Virus du SRAS (pathogénicité)</term>
<term>Virus du SRAS (physiologie)</term>
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<term>Poumon</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virus du SRAS</term>
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<term>Lung</term>
<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
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<front><div type="abstract" xml:lang="en"><p>Severe acute respiratory syndrome (SARS) is a zoonotic infectious disease caused by a novel coronavirus (CoV). The tissue tropism of SARS-CoV includes not only the lung, but also the gastrointestinal tract, kidney and liver. Angiotensin-converting enzyme 2 (ACE2), the C-type lectin CD209L (also known L-SIGN), and DC-SIGN bind SARS-CoV, but ACE2 appears to be the key functional receptor for the virus. There is a prominent innate immune response to SARS-CoV infection, including acute-phase proteins, chemokines, inflammatory cytokines and C-type lectins such as mannose-binding lectin, which plays a protective role against SARS. By contrast there may be a lack of type 1 interferon response. Moreover, lymphopenia with decreased numbers of CD4<sup>+</sup>
and CD8<sup>+</sup>
T cells is common during the acute phase. Convalescent patients have IgG-class neutralizing antibodies that recognize amino acids 441–700 of the spike protein (S protein) as the major epitope.</p>
</div>
</front>
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<double pmid="15950449"><pmc><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pathogenesis of severe acute respiratory syndrome</title>
<author><name sortKey="Lau, Yu Lung" sort="Lau, Yu Lung" uniqKey="Lau Y" first="Yu Lung" last="Lau">Yu Lung Lau</name>
<affiliation wicri:level="1"><nlm:aff id="aff1">Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Room 117 New Clinical Building, Queen Mary Hospital, Pokfulam Road, Hong Kong</nlm:aff>
<country xml:lang="fr">Hong Kong</country>
<wicri:regionArea>Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Room 117 New Clinical Building, Queen Mary Hospital, Pokfulam Road</wicri:regionArea>
<wicri:noRegion>Pokfulam Road</wicri:noRegion>
</affiliation>
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<author><name sortKey="Peiris, Js Malik" sort="Peiris, Js Malik" uniqKey="Peiris J" first="Js Malik" last="Peiris">Js Malik Peiris</name>
<affiliation wicri:level="1"><nlm:aff id="aff2">Department of Microbiology, The University of Hong Kong, Room 117 New Clinical Building, Queen Mary Hospital, Pokfulam Road, Hong Kong</nlm:aff>
<country xml:lang="fr">Hong Kong</country>
<wicri:regionArea>Department of Microbiology, The University of Hong Kong, Room 117 New Clinical Building, Queen Mary Hospital, Pokfulam Road</wicri:regionArea>
<wicri:noRegion>Pokfulam Road</wicri:noRegion>
</affiliation>
</author>
</titleStmt>
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<idno type="pmid">15950449</idno>
<idno type="pmc">7127490</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7127490</idno>
<idno type="RBID">PMC:7127490</idno>
<idno type="doi">10.1016/j.coi.2005.05.009</idno>
<date when="2005">2005</date>
<idno type="wicri:Area/Pmc/Corpus">001726</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001726</idno>
<idno type="wicri:Area/Pmc/Curation">001726</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">001726</idno>
<idno type="wicri:Area/Pmc/Checkpoint">001283</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">001283</idno>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Pathogenesis of severe acute respiratory syndrome</title>
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<affiliation wicri:level="1"><nlm:aff id="aff1">Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Room 117 New Clinical Building, Queen Mary Hospital, Pokfulam Road, Hong Kong</nlm:aff>
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<wicri:regionArea>Department of Microbiology, The University of Hong Kong, Room 117 New Clinical Building, Queen Mary Hospital, Pokfulam Road</wicri:regionArea>
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<idno type="eISSN">1879-0372</idno>
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<front><div type="abstract" xml:lang="en"><p>Severe acute respiratory syndrome (SARS) is a zoonotic infectious disease caused by a novel coronavirus (CoV). The tissue tropism of SARS-CoV includes not only the lung, but also the gastrointestinal tract, kidney and liver. Angiotensin-converting enzyme 2 (ACE2), the C-type lectin CD209L (also known L-SIGN), and DC-SIGN bind SARS-CoV, but ACE2 appears to be the key functional receptor for the virus. There is a prominent innate immune response to SARS-CoV infection, including acute-phase proteins, chemokines, inflammatory cytokines and C-type lectins such as mannose-binding lectin, which plays a protective role against SARS. By contrast there may be a lack of type 1 interferon response. Moreover, lymphopenia with decreased numbers of CD4<sup>+</sup>
and CD8<sup>+</sup>
T cells is common during the acute phase. Convalescent patients have IgG-class neutralizing antibodies that recognize amino acids 441–700 of the spike protein (S protein) as the major epitope.</p>
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<country xml:lang="fr">Hong Kong</country>
<wicri:regionArea>Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Room 117 New Clinical Building, Queen Mary Hospital, Pokfulam Road</wicri:regionArea>
<wicri:noRegion>Pokfulam Road</wicri:noRegion>
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<author><name sortKey="Peiris, J S Malik" sort="Peiris, J S Malik" uniqKey="Peiris J" first="J S Malik" last="Peiris">J S Malik Peiris</name>
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<affiliation wicri:level="1"><nlm:affiliation>Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Room 117 New Clinical Building, Queen Mary Hospital, Pokfulam Road, Hong Kong. lauylung@hkucc.hku.hk</nlm:affiliation>
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<author><name sortKey="Peiris, J S Malik" sort="Peiris, J S Malik" uniqKey="Peiris J" first="J S Malik" last="Peiris">J S Malik Peiris</name>
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<series><title level="j">Current opinion in immunology</title>
<idno type="ISSN">0952-7915</idno>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Genetic Predisposition to Disease</term>
<term>Humans</term>
<term>Immunity, Innate (immunology)</term>
<term>Lung (immunology)</term>
<term>Lung (pathology)</term>
<term>Lung (virology)</term>
<term>SARS Virus (immunology)</term>
<term>SARS Virus (pathogenicity)</term>
<term>SARS Virus (physiology)</term>
<term>Severe Acute Respiratory Syndrome (genetics)</term>
<term>Severe Acute Respiratory Syndrome (immunology)</term>
<term>Severe Acute Respiratory Syndrome (pathology)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
</keywords>
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<term>Humains</term>
<term>Immunité innée (immunologie)</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (immunologie)</term>
<term>Poumon (virologie)</term>
<term>Prédisposition génétique à une maladie</term>
<term>Syndrome respiratoire aigu sévère (anatomopathologie)</term>
<term>Syndrome respiratoire aigu sévère (génétique)</term>
<term>Syndrome respiratoire aigu sévère (immunologie)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Virus du SRAS (immunologie)</term>
<term>Virus du SRAS (pathogénicité)</term>
<term>Virus du SRAS (physiologie)</term>
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<term>Syndrome respiratoire aigu sévère</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Immunité innée</term>
<term>Poumon</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virus du SRAS</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Immunity, Innate</term>
<term>Lung</term>
<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term>
<term>Severe Acute Respiratory Syndrome</term>
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<term>Syndrome respiratoire aigu sévère</term>
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<term>Severe Acute Respiratory Syndrome</term>
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<term>Genetic Predisposition to Disease</term>
<term>Humans</term>
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<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is a zoonotic infectious disease caused by a novel coronavirus (CoV). The tissue tropism of SARS-CoV includes not only the lung, but also the gastrointestinal tract, kidney and liver. Angiotensin-converting enzyme 2 (ACE2), the C-type lectin CD209L (also known L-SIGN), and DC-SIGN bind SARS-CoV, but ACE2 appears to be the key functional receptor for the virus. There is a prominent innate immune response to SARS-CoV infection, including acute-phase proteins, chemokines, inflammatory cytokines and C-type lectins such as mannose-binding lectin, which plays a protective role against SARS. By contrast there may be a lack of type 1 interferon response. Moreover, lymphopenia with decreased numbers of CD4+ and CD8+ T cells is common during the acute phase. Convalescent patients have IgG-class neutralizing antibodies that recognize amino acids 441-700 of the spike protein (S protein) as the major epitope.</div>
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