Human immunopathogenesis of severe acute respiratory syndrome (SARS).
Identifieur interne : 001B19 ( PubMed/Checkpoint ); précédent : 001B18; suivant : 001B20Human immunopathogenesis of severe acute respiratory syndrome (SARS).
Auteurs : Mark J. Cameron [Canada] ; Jesus F. Bermejo-Martin ; Ali Danesh ; Matthew P. Muller ; David J. KelvinSource :
- Virus research [ 0168-1702 ] ; 2008.
Descripteurs français
- KwdFr :
- Cytokines (immunologie), Cytokines (métabolisme), Humains, Immunité innée, Interactions hôte-pathogène, Modèles biologiques, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (immunologie), Séquençage par oligonucléotides en batterie, Virus du SRAS (immunologie).
- MESH :
- anatomopathologie : Syndrome respiratoire aigu sévère.
- génétique : Syndrome respiratoire aigu sévère.
- immunologie : Cytokines, Syndrome respiratoire aigu sévère, Virus du SRAS.
- métabolisme : Cytokines.
- Humains, Immunité innée, Interactions hôte-pathogène, Modèles biologiques, Séquençage par oligonucléotides en batterie.
English descriptors
- KwdEn :
- Cytokines (immunology), Cytokines (metabolism), Host-Pathogen Interactions, Humans, Immunity, Innate, Models, Biological, Oligonucleotide Array Sequence Analysis, SARS Virus (immunology), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology).
- MESH :
- chemical , immunology : Cytokines.
- chemical , metabolism : Cytokines.
- genetics : Severe Acute Respiratory Syndrome.
- immunology : SARS Virus, Severe Acute Respiratory Syndrome.
- pathology : Severe Acute Respiratory Syndrome.
- Host-Pathogen Interactions, Humans, Immunity, Innate, Models, Biological, Oligonucleotide Array Sequence Analysis.
Abstract
Progressive immune-associated injury is a hallmark of severe acute respiratory syndrome (SARS). Viral evasion of innate immunity, hypercytokinemia and systemic immunopathology in the SARS coronavirus (SARS CoV) infected host have been suggested as possible mechanisms for the cause of severe pathology and morbidity in SARS patients. The molecular and cellular basis for how SARS CoV impacts the host immune system resulting in severe SARS, however, has not been elucidated. The variable clinical course of SARS may be the result of complex programs of host responses against the infectious agent. Therefore, the systematic analysis of innate and adaptive immune responses to SARS CoV is imperative in building as complete an immunological model as possible of host immunity and inflammatory responses during illness. Here we review recent advances in SARS immunopathogenesis research and present a summary of our findings regarding host responses in SARS patients. We contend that dysregulated type I and II interferon (IFN) responses during SARS may culminate in a failure of the switch from hyper-innate immunity to protective adaptive immune responses in the human host.
DOI: 10.1016/j.virusres.2007.02.014
PubMed: 17374415
Affiliations:
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pubmed:17374415Le document en format XML
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<front><div type="abstract" xml:lang="en">Progressive immune-associated injury is a hallmark of severe acute respiratory syndrome (SARS). Viral evasion of innate immunity, hypercytokinemia and systemic immunopathology in the SARS coronavirus (SARS CoV) infected host have been suggested as possible mechanisms for the cause of severe pathology and morbidity in SARS patients. The molecular and cellular basis for how SARS CoV impacts the host immune system resulting in severe SARS, however, has not been elucidated. The variable clinical course of SARS may be the result of complex programs of host responses against the infectious agent. Therefore, the systematic analysis of innate and adaptive immune responses to SARS CoV is imperative in building as complete an immunological model as possible of host immunity and inflammatory responses during illness. Here we review recent advances in SARS immunopathogenesis research and present a summary of our findings regarding host responses in SARS patients. We contend that dysregulated type I and II interferon (IFN) responses during SARS may culminate in a failure of the switch from hyper-innate immunity to protective adaptive immune responses in the human host.</div>
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<tree><noCountry><name sortKey="Bermejo Martin, Jesus F" sort="Bermejo Martin, Jesus F" uniqKey="Bermejo Martin J" first="Jesus F" last="Bermejo-Martin">Jesus F. Bermejo-Martin</name>
<name sortKey="Danesh, Ali" sort="Danesh, Ali" uniqKey="Danesh A" first="Ali" last="Danesh">Ali Danesh</name>
<name sortKey="Kelvin, David J" sort="Kelvin, David J" uniqKey="Kelvin D" first="David J" last="Kelvin">David J. Kelvin</name>
<name sortKey="Muller, Matthew P" sort="Muller, Matthew P" uniqKey="Muller M" first="Matthew P" last="Muller">Matthew P. Muller</name>
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<country name="Canada"><noRegion><name sortKey="Cameron, Mark J" sort="Cameron, Mark J" uniqKey="Cameron M" first="Mark J" last="Cameron">Mark J. Cameron</name>
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</affiliations>
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