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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pubmed:17451827Le document en format XML
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<term>Severe Acute Respiratory Syndrome</term>
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<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>
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