SrasV1, PubMed, Checkpoint, bibRecord, 000F78

Inhibition of NF-κB-mediated inflammation in severe acute respiratory syndrome coronavirus-infected mice increases survival.

Identifieur interne : 000F78 ( PubMed/Checkpoint ); précédent : 000F77; suivant : 000F79

Inhibition of NF-κB-mediated inflammation in severe acute respiratory syndrome coronavirus-infected mice increases survival.

Auteurs : Marta L. Dediego [Espagne] ; Jose L. Nieto-Torres ; Jose A. Regla-Nava ; Jose M. Jimenez-Guarde O ; Raul Fernandez-Delgado ; Craig Fett ; Carlos Casta O-Rodriguez ; Stanley Perlman ; Luis Enjuanes

Source :

Journal of virology [ 1098-5514 ] ; 2014.

RBID : pubmed:24198408

Descripteurs français

KwdFr :
- Animaux, Cytokines (génétique), Cytokines (immunologie), Facteur de transcription NF-kappa B (génétique), Facteur de transcription NF-kappa B (immunologie), Femelle, Humains, Protéines de l'enveloppe virale (génétique), Protéines de l'enveloppe virale (métabolisme), Régulation négative, Souris, Souris de lignée BALB C, Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (mortalité), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (génétique), Virus du SRAS (physiologie).
MESH :
- génétique : Cytokines, Facteur de transcription NF-kappa B, Protéines de l'enveloppe virale, Syndrome respiratoire aigu sévère, Virus du SRAS.
- immunologie : Cytokines, Facteur de transcription NF-kappa B, Syndrome respiratoire aigu sévère.
- mortalité : Syndrome respiratoire aigu sévère.
- métabolisme : Protéines de l'enveloppe virale.
- physiologie : Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Femelle, Humains, Régulation négative, Souris, Souris de lignée BALB C.

English descriptors

KwdEn :
- Animals, Cytokines (genetics), Cytokines (immunology), Down-Regulation, Female, Humans, Mice, Mice, Inbred BALB C, NF-kappa B (genetics), NF-kappa B (immunology), SARS Virus (genetics), SARS Virus (physiology), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (mortality), Severe Acute Respiratory Syndrome (virology), Viral Envelope Proteins (genetics), Viral Envelope Proteins (metabolism).
MESH :
- chemical , genetics : Cytokines, NF-kappa B, Viral Envelope Proteins.
- chemical , immunology : Cytokines, NF-kappa B.
- genetics : SARS Virus, Severe Acute Respiratory Syndrome.
- immunology : Severe Acute Respiratory Syndrome.
- chemical , metabolism : Viral Envelope Proteins.
- mortality : Severe Acute Respiratory Syndrome.
- physiology : SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Down-Regulation, Female, Humans, Mice, Mice, Inbred BALB C.

Abstract

Severe acute respiratory syndrome coronavirus (SARS-CoV) is the etiological agent of a respiratory disease that has a 10% mortality rate. We previously showed that SARS-CoV lacking the E gene (SARS-CoV-ΔE) is attenuated in several animal model systems. Here, we show that absence of the E protein resulted in reduced expression of proinflammatory cytokines, decreased numbers of neutrophils in lung infiltrates, diminished lung pathology, and increased mouse survival, suggesting that lung inflammation contributed to SARS-CoV virulence. Further, infection with SARS-CoV-ΔE resulted in decreased activation of NF-κB compared to levels for the wild-type virus. Most important, treatment with drugs that inhibited NF-κB activation led to a reduction in inflammation and lung pathology in both SARS-CoV-infected cultured cells and mice and significantly increased mouse survival after SARS-CoV infection. These data indicated that activation of the NF-κB signaling pathway represents a major contribution to the inflammation induced after SARS-CoV infection and that NF-κB inhibitors are promising antivirals in infections caused by SARS-CoV and potentially other pathogenic human coronaviruses.

DOI: 10.1128/JVI.02576-13
PubMed: 24198408

Affiliations:

Links toward previous steps (curation, corpus...)

to stream PubMed, to step Corpus: 001104
to stream PubMed, to step Curation: 001104

Links to Exploration step

pubmed:24198408

Le document en format XML

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<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome coronavirus (SARS-CoV) is the etiological agent of a respiratory disease that has a 10% mortality rate. We previously showed that SARS-CoV lacking the E gene (SARS-CoV-ΔE) is attenuated in several animal model systems. Here, we show that absence of the E protein resulted in reduced expression of proinflammatory cytokines, decreased numbers of neutrophils in lung infiltrates, diminished lung pathology, and increased mouse survival, suggesting that lung inflammation contributed to SARS-CoV virulence. Further, infection with SARS-CoV-ΔE resulted in decreased activation of NF-κB compared to levels for the wild-type virus. Most important, treatment with drugs that inhibited NF-κB activation led to a reduction in inflammation and lung pathology in both SARS-CoV-infected cultured cells and mice and significantly increased mouse survival after SARS-CoV infection. These data indicated that activation of the NF-κB signaling pathway represents a major contribution to the inflammation induced after SARS-CoV infection and that NF-κB inhibitors are promising antivirals in infections caused by SARS-CoV and potentially other pathogenic human coronaviruses. </div>
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Inhibition of NF-κB-mediated inflammation in severe acute respiratory syndrome coronavirus-infected mice increases survival.

Inhibition of NF-κB-mediated inflammation in severe acute respiratory syndrome coronavirus-infected mice increases survival.

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