Group 2 coronaviruses prevent immediate early interferon induction by protection of viral RNA from host cell recognition.
Identifieur interne : 001E91 ( PubMed/Curation ); précédent : 001E90; suivant : 001E92Group 2 coronaviruses prevent immediate early interferon induction by protection of viral RNA from host cell recognition.
Auteurs : Gijs A. Versteeg [Pays-Bas] ; Peter J. Bredenbeek ; Sjoerd H E. Van Den Worm ; Willy J M. SpaanSource :
- Virology [ 0042-6822 ] ; 2007.
Descripteurs français
- KwdFr :
- ARN viral (physiologie), Animaux, Cellules Vero, Facteur-3 de régulation d'interféron (métabolisme), Interféron alpha (métabolisme), Souris, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Transport biologique, Virus Sendai (immunologie), Virus de l'hépatite murine (immunologie), Virus du SRAS (génétique), Virus du SRAS (immunologie).
- MESH :
- génétique : Virus du SRAS.
- immunologie : Syndrome respiratoire aigu sévère, Virus Sendai, Virus de l'hépatite murine, Virus du SRAS.
- métabolisme : Facteur-3 de régulation d'interféron, Interféron alpha.
- physiologie : ARN viral.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Cellules Vero, Souris, Transport biologique.
English descriptors
- KwdEn :
- Animals, Biological Transport, Chlorocebus aethiops, Interferon Regulatory Factor-3 (metabolism), Interferon-alpha (metabolism), L Cells, Mice, Murine hepatitis virus (immunology), RNA, Viral (physiology), SARS Virus (genetics), SARS Virus (immunology), Sendai virus (immunology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), Vero Cells.
- MESH :
- chemical , metabolism : Interferon Regulatory Factor-3, Interferon-alpha.
- genetics : SARS Virus.
- immunology : Murine hepatitis virus, SARS Virus, Sendai virus, Severe Acute Respiratory Syndrome.
- chemical , physiology : RNA, Viral.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Biological Transport, Chlorocebus aethiops, L Cells, Mice, Vero Cells.
Abstract
Many viruses encode antagonists to prevent interferon (IFN) induction. Infection of fibroblasts with the murine hepatitis coronavirus (MHV) and SARS-coronavirus (SARS-CoV) did not result in nuclear translocation of interferon-regulatory factor 3 (IRF3), a key transcription factor involved in IFN induction, and induction of IFN mRNA transcription. Furthermore, MHV and SARS-CoV infection could not prevent IFN induction by poly (I:C) or Sendai virus, suggesting that these CoVs do not inactivate IRF3-mediated transcription regulation, but apparently prevent detection of replicative RNA by cellular sensory molecules. Our data indicate that shielding of viral RNA to host cell sensors might be the main general mechanism for coronaviruses to prevent IFN induction.
DOI: 10.1016/j.virol.2007.01.020
PubMed: 17316733
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pubmed:17316733Le document en format XML
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<term>Mice</term>
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<front><div type="abstract" xml:lang="en">Many viruses encode antagonists to prevent interferon (IFN) induction. Infection of fibroblasts with the murine hepatitis coronavirus (MHV) and SARS-coronavirus (SARS-CoV) did not result in nuclear translocation of interferon-regulatory factor 3 (IRF3), a key transcription factor involved in IFN induction, and induction of IFN mRNA transcription. Furthermore, MHV and SARS-CoV infection could not prevent IFN induction by poly (I:C) or Sendai virus, suggesting that these CoVs do not inactivate IRF3-mediated transcription regulation, but apparently prevent detection of replicative RNA by cellular sensory molecules. Our data indicate that shielding of viral RNA to host cell sensors might be the main general mechanism for coronaviruses to prevent IFN induction.</div>
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<Abstract><AbstractText>Many viruses encode antagonists to prevent interferon (IFN) induction. Infection of fibroblasts with the murine hepatitis coronavirus (MHV) and SARS-coronavirus (SARS-CoV) did not result in nuclear translocation of interferon-regulatory factor 3 (IRF3), a key transcription factor involved in IFN induction, and induction of IFN mRNA transcription. Furthermore, MHV and SARS-CoV infection could not prevent IFN induction by poly (I:C) or Sendai virus, suggesting that these CoVs do not inactivate IRF3-mediated transcription regulation, but apparently prevent detection of replicative RNA by cellular sensory molecules. Our data indicate that shielding of viral RNA to host cell sensors might be the main general mechanism for coronaviruses to prevent IFN induction.</AbstractText>
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