Severe acute respiratory syndrome coronavirus protein 6 is required for optimal replication.
Identifieur interne : 001E17 ( Ncbi/Checkpoint ); précédent : 001E16; suivant : 001E18Severe acute respiratory syndrome coronavirus protein 6 is required for optimal replication.
Auteurs : Jincun Zhao [États-Unis] ; Ana Falc N ; Haixia Zhou ; Jason Netland ; Luis Enjuanes ; Pilar Pérez Bre A ; Stanley PerlmanSource :
- Journal of virology [ 1098-5514 ] ; 2009.
Descripteurs français
- KwdFr :
- Animaux, Cadres ouverts de lecture, Facteur de transcription STAT-1 (métabolisme), Interféron gamma (pharmacologie), Lignée cellulaire, Protéines virales (métabolisme), Récepteurs viraux (métabolisme), Réplication virale, Souris, Souris transgéniques, Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (métabolisme), Virus du SRAS (pathogénicité), Virus du SRAS (physiologie).
- MESH :
- métabolisme : Facteur de transcription STAT-1, Protéines virales, Récepteurs viraux, Virus du SRAS.
- pathogénicité : Virus du SRAS.
- pharmacologie : Interféron gamma.
- physiologie : Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Cadres ouverts de lecture, Lignée cellulaire, Réplication virale, Souris, Souris transgéniques.
English descriptors
- KwdEn :
- Animals, Cell Line, Interferon-gamma (pharmacology), Mice, Mice, Transgenic, Open Reading Frames, Receptors, Virus (metabolism), SARS Virus (metabolism), SARS Virus (pathogenicity), SARS Virus (physiology), STAT1 Transcription Factor (metabolism), Severe Acute Respiratory Syndrome (virology), Viral Proteins (metabolism), Virus Replication.
- MESH :
- chemical , metabolism : Receptors, Virus, STAT1 Transcription Factor, Viral Proteins.
- chemical , pharmacology : Interferon-gamma.
- metabolism : SARS Virus.
- pathogenicity : SARS Virus.
- physiology : SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Cell Line, Mice, Mice, Transgenic, Open Reading Frames, Virus Replication.
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) encodes several accessory proteins of unknown function. One of these proteins, protein 6 (p6), which is encoded by ORF6, enhances virus replication when introduced into a heterologous murine coronavirus (mouse hepatitis virus [MHV]) but is not essential for optimal SARS-CoV replication after infection at a relatively high multiplicity of infection (MOI). Here, we reconcile these apparently conflicting results by showing that p6 enhances SARS-CoV replication to nearly the same extent as when expressed in the context of MHV if cells are infected at a low MOI and accelerates disease in mice transgenic for the human SARS-CoV receptor.
DOI: 10.1128/JVI.02371-08
PubMed: 19091867
Affiliations:
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pubmed:19091867Le document en format XML
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<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome coronavirus (SARS-CoV) encodes several accessory proteins of unknown function. One of these proteins, protein 6 (p6), which is encoded by ORF6, enhances virus replication when introduced into a heterologous murine coronavirus (mouse hepatitis virus [MHV]) but is not essential for optimal SARS-CoV replication after infection at a relatively high multiplicity of infection (MOI). Here, we reconcile these apparently conflicting results by showing that p6 enhances SARS-CoV replication to nearly the same extent as when expressed in the context of MHV if cells are infected at a low MOI and accelerates disease in mice transgenic for the human SARS-CoV receptor.</div>
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<name sortKey="Netland, Jason" sort="Netland, Jason" uniqKey="Netland J" first="Jason" last="Netland">Jason Netland</name>
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