Extraordinary GU-rich single-strand RNA identified from SARS coronavirus contributes an excessive innate immune response.
Identifieur interne : 001947 ( Main/Merge ); précédent : 001946; suivant : 001948Extraordinary GU-rich single-strand RNA identified from SARS coronavirus contributes an excessive innate immune response.
Auteurs : Yan Li [République populaire de Chine] ; Ming Chen ; Hongwei Cao ; Yuanfeng Zhu ; Jiang Zheng ; Hong ZhouSource :
- Microbes and infection [ 1769-714X ] ; 2013.
Descripteurs français
- KwdFr :
- ARN viral (administration et posologie), ARN viral (immunologie), Animaux, Biologie informatique (), Facteur de nécrose tumorale alpha (immunologie), Glycoprotéines membranaires (immunologie), Humains, Immunisation (), Immunité innée, Interactions hôte-pathogène, Interleukine-6 (immunologie), Lignée cellulaire tumorale, Lésion pulmonaire aigüe (anatomopathologie), Lésion pulmonaire aigüe (immunologie), Motifs nucléotidiques, Mâle, Petit ARN interférent (génétique), Petit ARN interférent (métabolisme), Récepteur de type Toll-7 (immunologie), Récepteur de type Toll-8 (immunologie), Souris, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Transfection, Virus du SRAS (génétique), Virus du SRAS (immunologie), Virus du SRAS (métabolisme).
- MESH :
- administration et posologie : ARN viral.
- anatomopathologie : Lésion pulmonaire aigüe, Syndrome respiratoire aigu sévère.
- génétique : Petit ARN interférent, Virus du SRAS.
- immunologie : ARN viral, Facteur de nécrose tumorale alpha, Glycoprotéines membranaires, Interleukine-6, Lésion pulmonaire aigüe, Récepteur de type Toll-7, Récepteur de type Toll-8, Syndrome respiratoire aigu sévère, Virus du SRAS.
- métabolisme : Petit ARN interférent, Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Biologie informatique, Humains, Immunisation, Immunité innée, Interactions hôte-pathogène, Lignée cellulaire tumorale, Motifs nucléotidiques, Mâle, Souris, Transfection.
English descriptors
- KwdEn :
- Acute Lung Injury (immunology), Acute Lung Injury (pathology), Animals, Cell Line, Tumor, Computational Biology (methods), Host-Pathogen Interactions, Humans, Immunity, Innate, Immunization (methods), Interleukin-6 (immunology), Male, Membrane Glycoproteins (immunology), Mice, Nucleotide Motifs, RNA, Small Interfering (genetics), RNA, Small Interfering (metabolism), RNA, Viral (administration & dosage), RNA, Viral (immunology), SARS Virus (genetics), SARS Virus (immunology), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Toll-Like Receptor 7 (immunology), Toll-Like Receptor 8 (immunology), Transfection, Tumor Necrosis Factor-alpha (immunology).
- MESH :
- chemical , administration & dosage : RNA, Viral.
- chemical , genetics : RNA, Small Interfering.
- chemical , immunology : Interleukin-6, Membrane Glycoproteins, RNA, Viral, Toll-Like Receptor 7, Toll-Like Receptor 8, Tumor Necrosis Factor-alpha.
- genetics : SARS Virus.
- immunology : Acute Lung Injury, SARS Virus, Severe Acute Respiratory Syndrome.
- chemical , metabolism : RNA, Small Interfering, SARS Virus.
- methods : Computational Biology, Immunization.
- pathology : Acute Lung Injury, Severe Acute Respiratory Syndrome.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Cell Line, Tumor, Host-Pathogen Interactions, Humans, Immunity, Innate, Male, Mice, Nucleotide Motifs, Transfection.
Abstract
A dangerous cytokine storm occurs in the SARS involving in immune disorder, but many aspects of the pathogenetic mechanism remain obscure since its outbreak. To deeply reveal the interaction of host and SARS-CoV, based on the basic structural feature of pathogen-associated molecular pattern, we created a new bioinformatics method for searching potential pathogenic molecules and identified a set of SARS-CoV specific GU-rich ssRNA fragments with a high-density distribution in the genome. In vitro experiments, the result showed the representative SARS-CoV ssRNAs had powerful immunostimulatory activities to induce considerable level of pro-inflammatory cytokine TNF-a, IL-6 and IL-12 release via the TLR7 and TLR8, almost 2-fold higher than the strong stimulatory ssRNA40 that was found previously from other virus. Moreover, SARS-CoV ssRNA was able to cause acute lung injury in mice with a high mortality rate in vivo experiment. It suggests that SARS-CoV specific GU-rich ssRNA plays a very important role in the cytokine storm associated with a dysregulation of the innate immunity. This study not only presents new evidence about the immunopathologic damage caused by overactive inflammation during the SARS-CoV infection, but also provides a useful clue for a new therapeutic strategy.
DOI: 10.1016/j.micinf.2012.10.008
PubMed: 23123977
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pubmed:23123977Le document en format XML
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<term>Cell Line, Tumor</term>
<term>Computational Biology (methods)</term>
<term>Host-Pathogen Interactions</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>Immunization (methods)</term>
<term>Interleukin-6 (immunology)</term>
<term>Male</term>
<term>Membrane Glycoproteins (immunology)</term>
<term>Mice</term>
<term>Nucleotide Motifs</term>
<term>RNA, Small Interfering (genetics)</term>
<term>RNA, Small Interfering (metabolism)</term>
<term>RNA, Viral (administration & dosage)</term>
<term>RNA, Viral (immunology)</term>
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<term>SARS Virus (immunology)</term>
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<term>Severe Acute Respiratory Syndrome (pathology)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Toll-Like Receptor 7 (immunology)</term>
<term>Toll-Like Receptor 8 (immunology)</term>
<term>Transfection</term>
<term>Tumor Necrosis Factor-alpha (immunology)</term>
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<term>ARN viral (immunologie)</term>
<term>Animaux</term>
<term>Biologie informatique ()</term>
<term>Facteur de nécrose tumorale alpha (immunologie)</term>
<term>Glycoprotéines membranaires (immunologie)</term>
<term>Humains</term>
<term>Immunisation ()</term>
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<term>Interactions hôte-pathogène</term>
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<term>Lignée cellulaire tumorale</term>
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<term>Lésion pulmonaire aigüe (immunologie)</term>
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<term>Mâle</term>
<term>Petit ARN interférent (génétique)</term>
<term>Petit ARN interférent (métabolisme)</term>
<term>Récepteur de type Toll-7 (immunologie)</term>
<term>Récepteur de type Toll-8 (immunologie)</term>
<term>Souris</term>
<term>Syndrome respiratoire aigu sévère (anatomopathologie)</term>
<term>Syndrome respiratoire aigu sévère (immunologie)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
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<term>Virus du SRAS (immunologie)</term>
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<term>Membrane Glycoproteins</term>
<term>RNA, Viral</term>
<term>Toll-Like Receptor 7</term>
<term>Toll-Like Receptor 8</term>
<term>Tumor Necrosis Factor-alpha</term>
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<term>Syndrome respiratoire aigu sévère</term>
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<term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>ARN viral</term>
<term>Facteur de nécrose tumorale alpha</term>
<term>Glycoprotéines membranaires</term>
<term>Interleukine-6</term>
<term>Lésion pulmonaire aigüe</term>
<term>Récepteur de type Toll-7</term>
<term>Récepteur de type Toll-8</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virus du SRAS</term>
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<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
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<term>SARS Virus</term>
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<term>Immunization</term>
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<term>Host-Pathogen Interactions</term>
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<term>Humains</term>
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<term>Immunité innée</term>
<term>Interactions hôte-pathogène</term>
<term>Lignée cellulaire tumorale</term>
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<front><div type="abstract" xml:lang="en">A dangerous cytokine storm occurs in the SARS involving in immune disorder, but many aspects of the pathogenetic mechanism remain obscure since its outbreak. To deeply reveal the interaction of host and SARS-CoV, based on the basic structural feature of pathogen-associated molecular pattern, we created a new bioinformatics method for searching potential pathogenic molecules and identified a set of SARS-CoV specific GU-rich ssRNA fragments with a high-density distribution in the genome. In vitro experiments, the result showed the representative SARS-CoV ssRNAs had powerful immunostimulatory activities to induce considerable level of pro-inflammatory cytokine TNF-a, IL-6 and IL-12 release via the TLR7 and TLR8, almost 2-fold higher than the strong stimulatory ssRNA40 that was found previously from other virus. Moreover, SARS-CoV ssRNA was able to cause acute lung injury in mice with a high mortality rate in vivo experiment. It suggests that SARS-CoV specific GU-rich ssRNA plays a very important role in the cytokine storm associated with a dysregulation of the innate immunity. This study not only presents new evidence about the immunopathologic damage caused by overactive inflammation during the SARS-CoV infection, but also provides a useful clue for a new therapeutic strategy.</div>
</front>
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