Serveur d'exploration SRAS

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Pathogenesis of severe acute respiratory syndrome

Identifieur interne : 001005 ( Ncbi/Merge ); précédent : 001004; suivant : 001006

Pathogenesis of severe acute respiratory syndrome

Auteurs : Yu Lung Lau [Hong Kong] ; Js Malik Peiris [Hong Kong]

Source :

RBID : PMC:7127490

Descripteurs français

English descriptors

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

Links toward previous steps (curation, corpus...)


Links to Exploration step

PMC:7127490

Le document en format XML

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<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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<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>
</analytic>
<series>
<title level="j">Current Opinion in Immunology</title>
<idno type="ISSN">0952-7915</idno>
<idno type="eISSN">1879-0372</idno>
<imprint>
<date when="2005">2005</date>
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<profileDesc>
<textClass></textClass>
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</teiHeader>
<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>
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<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>Animaux</term>
<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>
</keywords>
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<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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<term>Immunity, Innate</term>
<term>Lung</term>
<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
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<term>SARS Virus</term>
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<term>Virus du SRAS</term>
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<term>Lung</term>
<term>Severe Acute Respiratory Syndrome</term>
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<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr">
<term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en">
<term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr">
<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>Animals</term>
<term>Genetic Predisposition to Disease</term>
<term>Humans</term>
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<term>Animaux</term>
<term>Humains</term>
<term>Prédisposition génétique à une maladie</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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