Pathogenesis of severe acute respiratory syndrome.
Identifieur interne : 002689 ( PubMed/Curation ); précédent : 002688; suivant : 002690Pathogenesis of severe acute respiratory syndrome.
Auteurs : Yu Lung Lau [Hong Kong] ; J S Malik PeirisSource :
- 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.
DOI: 10.1016/j.coi.2005.05.009
PubMed: 15950449
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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></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Genetic Predisposition to Disease</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Prédisposition génétique à une maladie</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15950449</PMID><DateCompleted><Year>2005</Year><Month>11</Month><Day>01</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>10</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0952-7915</ISSN><JournalIssue CitedMedium="Print"><Volume>17</Volume><Issue>4</Issue><PubDate><Year>2005</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Current opinion in immunology</Title><ISOAbbreviation>Curr. Opin. Immunol.</ISOAbbreviation></Journal><ArticleTitle>Pathogenesis of severe acute respiratory syndrome.</ArticleTitle><Pagination><MedlinePgn>404-10</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lau</LastName><ForeName>Yu Lung</ForeName><Initials>YL</Initials><AffiliationInfo><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</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Peiris</LastName><ForeName>J S Malik</ForeName><Initials>JS</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>N01AI95357</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI95357</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United 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HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i -Sk "pubmed:15950449" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \
| NlmPubMed2Wicri -a SrasV1
| This area was generated with Dilib version V0.6.33. |  |