SARS coronavirus and innate immunity.
Identifieur interne : 001E43 ( PubMed/Curation ); précédent : 001E42; suivant : 001E44SARS coronavirus and innate immunity.
Auteurs : Matthew Frieman [États-Unis] ; Mark Heise ; Ralph BaricSource :
- Virus research [ 0168-1702 ] ; 2008.
Descripteurs français
- KwdFr :
- Animaux, Cellules Caco-2, Cellules dendritiques (immunologie), Cellules dendritiques (virologie), Génome viral, Humains, Immunité innée, Interactions hôte-pathogène, Interféron de type I (génétique), Interféron de type I (immunologie), Interféron de type I (métabolisme), Macrophages (immunologie), Macrophages (virologie), Réplication virale, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (croissance et développement), Virus du SRAS (immunologie), Virus du SRAS (physiologie).
- MESH :
- croissance et développement : Virus du SRAS.
- génétique : Interféron de type I.
- immunologie : Cellules dendritiques, Interféron de type I, Macrophages, Syndrome respiratoire aigu sévère, Virus du SRAS.
- métabolisme : Interféron de type I.
- physiologie : Virus du SRAS.
- virologie : Cellules dendritiques, Macrophages, Syndrome respiratoire aigu sévère.
- Animaux, Cellules Caco-2, Génome viral, Humains, Immunité innée, Interactions hôte-pathogène, Réplication virale.
English descriptors
- KwdEn :
- Animals, Caco-2 Cells, Dendritic Cells (immunology), Dendritic Cells (virology), Genome, Viral, Host-Pathogen Interactions, Humans, Immunity, Innate, Interferon Type I (genetics), Interferon Type I (immunology), Interferon Type I (metabolism), Macrophages (immunology), Macrophages (virology), SARS Virus (growth & development), SARS Virus (immunology), SARS Virus (physiology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), Virus Replication.
- MESH :
- chemical , genetics : Interferon Type I.
- growth & development : SARS Virus.
- immunology : Dendritic Cells, Interferon Type I, Macrophages, SARS Virus, Severe Acute Respiratory Syndrome.
- chemical , metabolism : Interferon Type I.
- physiology : SARS Virus.
- virology : Dendritic Cells, Macrophages, Severe Acute Respiratory Syndrome.
- Animals, Caco-2 Cells, Genome, Viral, Host-Pathogen Interactions, Humans, Immunity, Innate, Virus Replication.
Abstract
The emergence of the highly pathogenic SARS coronavirus (SARS-CoV) has reignited interest in coronavirus biology and pathogenesis. An emerging theme in coronavirus pathogenesis is that the interaction between specific viral genes and the host immune system, specifically the innate immune system, functions as a key determinant in regulating virulence and disease outcomes. Using SARS-CoV as a model, we will review the current knowledge of the interplay between coronavirus infection and the host innate immune system in vivo, and then discuss the mechanisms by which specific gene products antagonize the host innate immune response in cell culture models. Our data suggests that the SARS-CoV uses specific strategies to evade and antagonize the sensing and signaling arms of the interferon pathway. We summarize by identifying future points of consideration that will contribute greatly to our understanding of the molecular mechanisms governing coronavirus pathogenesis and virulence, and the development of severe disease in humans and animals.
DOI: 10.1016/j.virusres.2007.03.015
PubMed: 17451827
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SRAS (croissance et développement)</term><term>Virus du SRAS (immunologie)</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interferon Type I</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Interféron de type I</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules dendritiques</term><term>Interféron de type I</term><term>Macrophages</term><term>Syndrome respiratoire aigu sévère</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Dendritic Cells</term><term>Interferon Type I</term><term>Macrophages</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interferon Type I</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Interféron de type I</term></keywords><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>Cellules dendritiques</term><term>Macrophages</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Dendritic Cells</term><term>Macrophages</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Caco-2 Cells</term><term>Genome, Viral</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Immunity, Innate</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules Caco-2</term><term>Génome viral</term><term>Humains</term><term>Immunité innée</term><term>Interactions hôte-pathogène</term><term>Réplication virale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The emergence of the highly pathogenic SARS coronavirus (SARS-CoV) has reignited interest in coronavirus biology and pathogenesis. An emerging theme in coronavirus pathogenesis is that the interaction between specific viral genes and the host immune system, specifically the innate immune system, functions as a key determinant in regulating virulence and disease outcomes. Using SARS-CoV as a model, we will review the current knowledge of the interplay between coronavirus infection and the host innate immune system in vivo, and then discuss the mechanisms by which specific gene products antagonize the host innate immune response in cell culture models. Our data suggests that the SARS-CoV uses specific strategies to evade and antagonize the sensing and signaling arms of the interferon pathway. We summarize by identifying future points of consideration that will contribute greatly to our understanding of the molecular mechanisms governing coronavirus pathogenesis and virulence, and the development of severe disease in humans and animals.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17451827</PMID><DateCompleted><Year>2008</Year><Month>06</Month><Day>17</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0168-1702</ISSN><JournalIssue CitedMedium="Print"><Volume>133</Volume><Issue>1</Issue><PubDate><Year>2008</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Virus research</Title><ISOAbbreviation>Virus Res.</ISOAbbreviation></Journal><ArticleTitle>SARS coronavirus and innate immunity.</ArticleTitle><Pagination><MedlinePgn>101-12</MedlinePgn></Pagination><Abstract><AbstractText>The emergence of the highly pathogenic SARS coronavirus (SARS-CoV) has reignited interest in coronavirus biology and pathogenesis. An emerging theme in coronavirus pathogenesis is that the interaction between specific viral genes and the host immune system, specifically the innate immune system, functions as a key determinant in regulating virulence and disease outcomes. Using SARS-CoV as a model, we will review the current knowledge of the interplay between coronavirus infection and the host innate immune system in vivo, and then discuss the mechanisms by which specific gene products antagonize the host innate immune response in cell culture models. Our data suggests that the SARS-CoV uses specific strategies to evade and antagonize the sensing and signaling arms of the interferon pathway. We summarize by identifying future points of consideration that will contribute greatly to our understanding of the molecular mechanisms governing coronavirus pathogenesis and virulence, and the development of severe disease in humans and animals.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Frieman</LastName><ForeName>Matthew</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States. frieman@email.unc.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heise</LastName><ForeName>Mark</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Baric</LastName><ForeName>Ralph</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>F32 AI066542</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>F32 AI066542-03</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>04</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Virus Res</MedlineTA><NlmUniqueID>8410979</NlmUniqueID><ISSNLinking>0168-1702</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007370">Interferon Type I</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018938" MajorTopicYN="N">Caco-2 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003713" MajorTopicYN="N">Dendritic Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016679" MajorTopicYN="N">Genome, Viral</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054884" MajorTopicYN="Y">Host-Pathogen Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="Y">Immunity, Innate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007370" MajorTopicYN="N">Interferon Type I</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus 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