SrasV1, Main, Exploration, bibRecord, 003065

Pathogenicity of severe acute respiratory coronavirus deletion mutants in hACE-2 transgenic mice.

Identifieur interne : 003065 ( Main/Exploration ); précédent : 003064; suivant : 003066

Pathogenicity of severe acute respiratory coronavirus deletion mutants in hACE-2 transgenic mice.

Auteurs : Marta L. Dediego [Espagne] ; Lecia Pewe ; Enrique Alvarez ; Maria Teresa Rejas ; Stanley Perlman ; Luis Enjuanes

Source :

Virology [ 0042-6822 ] ; 2008.

RBID : pubmed:18452964

Descripteurs français

KwdFr :
- Animaux, Délétion de gène, Facteurs de transcription (physiologie), Facteurs de virulence, Humains, Lignée cellulaire, Peptidyl-Dipeptidase A (génétique), Protéines de liaison à l'ADN (physiologie), Souris, Souris de lignée C57BL, Souris transgéniques, Syndrome respiratoire aigu sévère (virologie), Virulence, Virus du SRAS (génétique), Virus du SRAS (pathogénicité).
MESH :
- génétique : Peptidyl-Dipeptidase A, Virus du SRAS.
- pathogénicité : Virus du SRAS.
- physiologie : Facteurs de transcription, Protéines de liaison à l'ADN.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Délétion de gène, Facteurs de virulence, Humains, Lignée cellulaire, Souris, Souris de lignée C57BL, Souris transgéniques, Virulence.

English descriptors

KwdEn :
- Animals, Cell Line, DNA-Binding Proteins (physiology), Gene Deletion, Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic, Peptidyl-Dipeptidase A (genetics), SARS Virus (genetics), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (virology), Transcription Factors (physiology), Virulence, Virulence Factors.
MESH :
- chemical , genetics : Peptidyl-Dipeptidase A.
- chemical , physiology : DNA-Binding Proteins, Transcription Factors.
- genetics : SARS Virus.
- pathogenicity : SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Cell Line, Gene Deletion, Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic, Virulence, Virulence Factors.

Abstract

Recombinant severe acute respiratory virus (SARS-CoV) variants lacking the group specific genes 6, 7a, 7b, 8a, 8b and 9b (rSARS-CoV-Delta[6-9b]), the structural gene E (rSARS-CoV-DeltaE), and a combination of both sets of genes (rSARS-CoV-Delta[E,6-9b]) have been generated. All these viruses were rescued in monkey (Vero E6) cells and were also infectious for human (Huh-7, Huh7.5.1 and CaCo-2) cell lines and for transgenic (Tg) mice expressing the SARS-CoV receptor human angiotensin converting enzyme-2 (hACE-2), indicating that none of these proteins is essential for the viral cycle. Furthermore, in Vero E6 cells, all the viruses showed the formation of particles with the same morphology as the wt virus, indicating that these proteins do not have a high impact in the final morphology of the virions. Nevertheless, in the absence of E protein, release of virus particles efficacy was reduced. Viruses lacking E protein grew about 100-fold lower than the wt virus in lungs of Tg infected mice but did not grow in the brains of the same animals, in contrast to the rSARS-CoV-Delta[6-9b] virus, which grew almost as well as the wt in both tissues. Viruses lacking E protein were highly attenuated in the highly sensitive hACE-2 Tg mice, in contrast to the minimal rSARS-CoV-Delta[6-9b] and wt viruses. These data indicate that E gene might be a virulence factor influencing replication level, tissue tropism and pathogenicity of SARS-CoV, suggesting that DeltaE attenuated viruses are promising vaccine candidates.

DOI: 10.1016/j.virol.2008.03.005
PubMed: 18452964

Affiliations:

Le document en format XML

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<wicri:regionArea>Department of Molecular and Cell Biology, Centro Nacional de Biotecnología (CSIC), Campus Universidad Autónoma, Darwin 3, Cantoblanco, 28049 Madrid</wicri:regionArea>
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<term>Cell Line</term>
<term>DNA-Binding Proteins (physiology)</term>
<term>Gene Deletion</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Transgenic</term>
<term>Peptidyl-Dipeptidase A (genetics)</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (pathogenicity)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Transcription Factors (physiology)</term>
<term>Virulence</term>
<term>Virulence Factors</term>
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<term>Délétion de gène</term>
<term>Facteurs de transcription (physiologie)</term>
<term>Facteurs de virulence</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Peptidyl-Dipeptidase A (génétique)</term>
<term>Protéines de liaison à l'ADN (physiologie)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris transgéniques</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Virulence</term>
<term>Virus du SRAS (génétique)</term>
<term>Virus du SRAS (pathogénicité)</term>
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<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Peptidyl-Dipeptidase A</term>
<term>Virus du SRAS</term>
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<term>Protéines de liaison à l'ADN</term>
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<term>Lignée cellulaire</term>
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<front><div type="abstract" xml:lang="en">Recombinant severe acute respiratory virus (SARS-CoV) variants lacking the group specific genes 6, 7a, 7b, 8a, 8b and 9b (rSARS-CoV-Delta[6-9b]), the structural gene E (rSARS-CoV-DeltaE), and a combination of both sets of genes (rSARS-CoV-Delta[E,6-9b]) have been generated. All these viruses were rescued in monkey (Vero E6) cells and were also infectious for human (Huh-7, Huh7.5.1 and CaCo-2) cell lines and for transgenic (Tg) mice expressing the SARS-CoV receptor human angiotensin converting enzyme-2 (hACE-2), indicating that none of these proteins is essential for the viral cycle. Furthermore, in Vero E6 cells, all the viruses showed the formation of particles with the same morphology as the wt virus, indicating that these proteins do not have a high impact in the final morphology of the virions. Nevertheless, in the absence of E protein, release of virus particles efficacy was reduced. Viruses lacking E protein grew about 100-fold lower than the wt virus in lungs of Tg infected mice but did not grow in the brains of the same animals, in contrast to the rSARS-CoV-Delta[6-9b] virus, which grew almost as well as the wt in both tissues. Viruses lacking E protein were highly attenuated in the highly sensitive hACE-2 Tg mice, in contrast to the minimal rSARS-CoV-Delta[6-9b] and wt viruses. These data indicate that E gene might be a virulence factor influencing replication level, tissue tropism and pathogenicity of SARS-CoV, suggesting that DeltaE attenuated viruses are promising vaccine candidates.</div>
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Pathogenicity of severe acute respiratory coronavirus deletion mutants in hACE-2 transgenic mice.

Pathogenicity of severe acute respiratory coronavirus deletion mutants in hACE-2 transgenic mice.

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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