SrasV1, Ncbi, Merge, bibRecord, 001A36

Severe acute respiratory syndrome coronavirus gene 7 products contribute to virus-induced apoptosis.

Identifieur interne : 001A36 ( Ncbi/Merge ); précédent : 001A35; suivant : 001A37

Severe acute respiratory syndrome coronavirus gene 7 products contribute to virus-induced apoptosis.

Auteurs : Scott R. Schaecher [États-Unis] ; Erin Touchette ; Jill Schriewer ; R Mark Buller ; Andrew Pekosz

Source :

Journal of virology [ 0022-538X ] ; 2007.

RBID : pubmed:17686858

Descripteurs français

KwdFr :
- Animaux, Apoptose, Cadres ouverts de lecture (physiologie), Cricetinae, Délétion de séquence, Humains, Lignée de cellules transformées, Mesocricetus, Méthode TUNEL, Protéines virales (génétique), Protéines virales (physiologie), Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (physiologie).
MESH :
- anatomopathologie : Syndrome respiratoire aigu sévère.
- génétique : Protéines virales.
- physiologie : Cadres ouverts de lecture, Protéines virales, Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Apoptose, Cricetinae, Délétion de séquence, Humains, Lignée de cellules transformées, Mesocricetus, Méthode TUNEL.

English descriptors

KwdEn :
- Animals, Apoptosis, Cell Line, Transformed, Cricetinae, Humans, In Situ Nick-End Labeling, Mesocricetus, Open Reading Frames (physiology), SARS Virus (physiology), Sequence Deletion, Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Viral Proteins (genetics), Viral Proteins (physiology).
MESH :
- chemical , genetics : Viral Proteins.
- pathology : Severe Acute Respiratory Syndrome.
- physiology : Open Reading Frames, SARS Virus, Viral Proteins.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Apoptosis, Cell Line, Transformed, Cricetinae, Humans, In Situ Nick-End Labeling, Mesocricetus, Sequence Deletion.

Abstract

The proteins encoded by gene 7 of the severe acute respiratory syndrome coronavirus (SARS-CoV) have been demonstrated to have proapoptotic activity when expressed from cDNA but appear to be dispensable for virus replication. Recombinant SARS-CoVs bearing deletions in gene 7 were used to assess the contribution of gene 7 to virus replication and apoptosis in several transformed cell lines, as well as to replication and pathogenesis in golden Syrian hamsters. Deletion of gene 7 had no effect on SARS-CoV replication in transformed cell lines, nor did it alter the induction of early apoptosis markers such as annexin V binding and activation of caspase 3. However, viruses with gene 7 disruptions were not as efficient as wild-type virus in inducing DNA fragmentation, as judged by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) staining, indicating that the gene 7 products do contribute to virus-induced apoptosis. Disruption of gene 7 did not affect virus replication or morbidity in golden Syrian hamsters, suggesting that the gene 7 products are not required for acute infection in vivo. The data indicate that open reading frames 7a and 7b contribute to but are not solely responsible for the apoptosis seen in SARS-CoV-infected cells.

DOI: 10.1128/JVI.01266-07
PubMed: 17686858

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pubmed:17686858

Le document en format XML

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<front><div type="abstract" xml:lang="en">The proteins encoded by gene 7 of the severe acute respiratory syndrome coronavirus (SARS-CoV) have been demonstrated to have proapoptotic activity when expressed from cDNA but appear to be dispensable for virus replication. Recombinant SARS-CoVs bearing deletions in gene 7 were used to assess the contribution of gene 7 to virus replication and apoptosis in several transformed cell lines, as well as to replication and pathogenesis in golden Syrian hamsters. Deletion of gene 7 had no effect on SARS-CoV replication in transformed cell lines, nor did it alter the induction of early apoptosis markers such as annexin V binding and activation of caspase 3. However, viruses with gene 7 disruptions were not as efficient as wild-type virus in inducing DNA fragmentation, as judged by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) staining, indicating that the gene 7 products do contribute to virus-induced apoptosis. Disruption of gene 7 did not affect virus replication or morbidity in golden Syrian hamsters, suggesting that the gene 7 products are not required for acute infection in vivo. The data indicate that open reading frames 7a and 7b contribute to but are not solely responsible for the apoptosis seen in SARS-CoV-infected cells.</div>
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<Abstract><AbstractText>The proteins encoded by gene 7 of the severe acute respiratory syndrome coronavirus (SARS-CoV) have been demonstrated to have proapoptotic activity when expressed from cDNA but appear to be dispensable for virus replication. Recombinant SARS-CoVs bearing deletions in gene 7 were used to assess the contribution of gene 7 to virus replication and apoptosis in several transformed cell lines, as well as to replication and pathogenesis in golden Syrian hamsters. Deletion of gene 7 had no effect on SARS-CoV replication in transformed cell lines, nor did it alter the induction of early apoptosis markers such as annexin V binding and activation of caspase 3. However, viruses with gene 7 disruptions were not as efficient as wild-type virus in inducing DNA fragmentation, as judged by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) staining, indicating that the gene 7 products do contribute to virus-induced apoptosis. Disruption of gene 7 did not affect virus replication or morbidity in golden Syrian hamsters, suggesting that the gene 7 products are not required for acute infection in vivo. The data indicate that open reading frames 7a and 7b contribute to but are not solely responsible for the apoptosis seen in SARS-CoV-infected cells.</AbstractText>
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Severe acute respiratory syndrome coronavirus gene 7 products contribute to virus-induced apoptosis.

Severe acute respiratory syndrome coronavirus gene 7 products contribute to virus-induced apoptosis.

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