SrasV1, Main, Exploration, bibRecord, 003D13

Severe Acute Respiratory Syndrome Coronavirus Protein 6 Accelerates Murine Coronavirus Infections▿

Identifieur interne : 003D13 ( Main/Exploration ); précédent : 003D12; suivant : 003D14

Severe Acute Respiratory Syndrome Coronavirus Protein 6 Accelerates Murine Coronavirus Infections▿

Auteurs : Chandra Tangudu ; Heidi Olivares ; Jason Netland ; Stanley Perlman ; Thomas Gallagher

Source :

Journal of Virology [ 0022-538X ] ; 2006.

RBID : PMC:1797517

Descripteurs français

KwdFr :
- Animaux, Cadres ouverts de lecture (génétique), Cellules HeLa, Humains, Infections à coronavirus (médecine vétérinaire), Infections à coronavirus (virologie), Protéines virales non structurales (génétique), Protéines virales non structurales (physiologie), Réplication virale (physiologie), Souris, Virulence (génétique), Virus du SRAS ().
MESH :
- génétique : Cadres ouverts de lecture, Protéines virales non structurales, Virulence.
- médecine vétérinaire : Infections à coronavirus.
- physiologie : Protéines virales non structurales, Réplication virale.
- virologie : Infections à coronavirus.
- Animaux, Cellules HeLa, Humains, Souris, Virus du SRAS.

English descriptors

KwdEn :
- Animals, Coronavirus Infections (veterinary), Coronavirus Infections (virology), HeLa Cells, Humans, Mice, Open Reading Frames (genetics), SARS Virus (chemistry), Viral Nonstructural Proteins (genetics), Viral Nonstructural Proteins (physiology), Virulence (genetics), Virus Replication (physiology).
MESH :
- chemical , genetics : Viral Nonstructural Proteins.
- chemistry : SARS Virus.
- genetics : Open Reading Frames, Virulence.
- chemical , physiology : Viral Nonstructural Proteins, Virus Replication.
- veterinary : Coronavirus Infections.
- virology : Coronavirus Infections.
- Animals, HeLa Cells, Humans, Mice.

Abstract

One or more of the unique 3′-proximal open reading frames (ORFs) of the severe acute respiratory syndrome (SARS) coronavirus may encode determinants of virus virulence. A prime candidate is ORF6, which encodes a 63-amino-acid membrane-associated peptide that can dramatically increase the lethality of an otherwise attenuated JHM strain of murine coronavirus (L. Pewe, H. Zhou, J. Netland, C. Tangudu, H. Olivares, L. Shi, D. Look, T. Gallagher, and S. Perlman, J. Virol. 79:11335-11342, 2005). To discern virulence mechanisms, we compared the in vitro growth properties of rJ.6, a recombinant JHM expressing the SARS peptide, with isogenic rJ.6-KO, which has an inactive ORF containing a mutated initiation codon and a termination codon at internal position 27. The rJ.6 infections proceeded rapidly, secreting progeny about 1.5 h earlier than rJ.6-KO infections did. The rJ.6 infections were also set apart by early viral protein accumulation and by robust expansion via syncytia, a characteristic feature of JHM virus dissemination. We found no evidence for protein 6 operating at the virus entry or assembly stage, as virions from either infection were indistinguishable. Rather, protein 6 appeared to operate by fostering viral RNA and protein synthesis, as RNA quantifications by reverse transcription-quantitative PCR revealed viral RNA levels in the rJ.6 cultures that were five to eight times higher than those lacking protein 6. Furthermore, protein 6 coimmunoprecipitated with viral RNAs and colocalized on cytoplasmic vesicles with replicating viral RNAs. The SARS coronavirus encodes a novel membrane protein 6 that can accelerate replication of a related mouse virus, a property that may explain its ability to increase in vivo virus virulence.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1797517

DOI: 10.1128/JVI.01515-06
PubMed: 17108045
PubMed Central: 1797517

Affiliations:

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<front><div type="abstract" xml:lang="en"><p>One or more of the unique 3′-proximal open reading frames (ORFs) of the severe acute respiratory syndrome (SARS) coronavirus may encode determinants of virus virulence. A prime candidate is ORF6, which encodes a 63-amino-acid membrane-associated peptide that can dramatically increase the lethality of an otherwise attenuated JHM strain of murine coronavirus (L. Pewe, H. Zhou, J. Netland, C. Tangudu, H. Olivares, L. Shi, D. Look, T. Gallagher, and S. Perlman, J. Virol. 79:11335-11342, 2005). To discern virulence mechanisms, we compared the in vitro growth properties of rJ.6, a recombinant JHM expressing the SARS peptide, with isogenic rJ.6-KO, which has an inactive ORF containing a mutated initiation codon and a termination codon at internal position 27. The rJ.6 infections proceeded rapidly, secreting progeny about 1.5 h earlier than rJ.6-KO infections did. The rJ.6 infections were also set apart by early viral protein accumulation and by robust expansion via syncytia, a characteristic feature of JHM virus dissemination. We found no evidence for protein 6 operating at the virus entry or assembly stage, as virions from either infection were indistinguishable. Rather, protein 6 appeared to operate by fostering viral RNA and protein synthesis, as RNA quantifications by reverse transcription-quantitative PCR revealed viral RNA levels in the rJ.6 cultures that were five to eight times higher than those lacking protein 6. Furthermore, protein 6 coimmunoprecipitated with viral RNAs and colocalized on cytoplasmic vesicles with replicating viral RNAs. The SARS coronavirus encodes a novel membrane protein 6 that can accelerate replication of a related mouse virus, a property that may explain its ability to increase in vivo virus virulence.</p>
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Severe Acute Respiratory Syndrome Coronavirus Protein 6 Accelerates Murine Coronavirus Infections▿

Severe Acute Respiratory Syndrome Coronavirus Protein 6 Accelerates Murine Coronavirus Infections▿

Source :

Descripteurs français

English descriptors

Abstract

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

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki

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