Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics.
Identifieur interne : 001154 ( Ncbi/Curation ); précédent : 001153; suivant : 001155Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics.
Auteurs : L. Bordi [Italie] ; C. Castilletti ; L. Falasca ; F. Ciccosanti ; S. Calcaterra ; G. Rozera ; A. Di Caro ; S. Zaniratti ; A. Rinaldi ; G. Ippolito ; M. Piacentini ; M R CapobianchiSource :
- Archives of virology [ 0304-8608 ] ; 2006.
Descripteurs français
- KwdFr :
- MESH :
- génétique : Protéines proto-oncogènes c-bcl-2.
- métabolisme : Caspases, Protéines proto-oncogènes c-bcl-2.
- pathogénicité : Virus du SRAS.
- physiologie : Virus du SRAS.
- Animaux, Apoptose, Cellules Vero, Facteurs temps, Réplication virale.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Proto-Oncogene Proteins c-bcl-2.
- chemical , metabolism : Caspases, Proto-Oncogene Proteins c-bcl-2.
- pathogenicity : SARS Virus.
- physiology : SARS Virus.
- Animals, Apoptosis, Chlorocebus aethiops, Time Factors, Vero Cells, Virus Replication.
Abstract
Vero cells transfected with either neo- or bcl-2-plasmid were infected with SARS-CoV at a high multiplicity of infection. Apoptosis appeared after the onset of CPE and completion of virus replication, and could be prevented by Bcl-2 expression. Apoptosis is likely mediated by the mitochondrial pathway, as demonstrated by its inhibition using Bcl-2, and by the activation of the caspase cascade, resulting in PARP cleavage. Prevention of apoptosis did not affect susceptibility to infection, kinetics and extent of viral replication and release, thus implying that apoptosis is not involved in facilitating release and/or dissemination of SARS-CoV in Vero cells.
DOI: 10.1007/s00705-005-0632-8
PubMed: 16155806
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pubmed:16155806Le document en format XML
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Falasca</name></author><author><name sortKey="Ciccosanti, F" sort="Ciccosanti, F" uniqKey="Ciccosanti F" first="F" last="Ciccosanti">F. Ciccosanti</name></author><author><name sortKey="Calcaterra, S" sort="Calcaterra, S" uniqKey="Calcaterra S" first="S" last="Calcaterra">S. Calcaterra</name></author><author><name sortKey="Rozera, G" sort="Rozera, G" uniqKey="Rozera G" first="G" last="Rozera">G. Rozera</name></author><author><name sortKey="Di Caro, A" sort="Di Caro, A" uniqKey="Di Caro A" first="A" last="Di Caro">A. Di Caro</name></author><author><name sortKey="Zaniratti, S" sort="Zaniratti, S" uniqKey="Zaniratti S" first="S" last="Zaniratti">S. Zaniratti</name></author><author><name sortKey="Rinaldi, A" sort="Rinaldi, A" uniqKey="Rinaldi A" first="A" last="Rinaldi">A. Rinaldi</name></author><author><name sortKey="Ippolito, G" sort="Ippolito, G" uniqKey="Ippolito G" first="G" last="Ippolito">G. Ippolito</name></author><author><name sortKey="Piacentini, M" sort="Piacentini, M" uniqKey="Piacentini M" first="M" last="Piacentini">M. Piacentini</name></author><author><name sortKey="Capobianchi, M R" sort="Capobianchi, M R" uniqKey="Capobianchi M" first="M R" last="Capobianchi">M R Capobianchi</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2006">2006</date><idno type="RBID">pubmed:16155806</idno><idno type="pmid">16155806</idno><idno type="doi">10.1007/s00705-005-0632-8</idno><idno type="wicri:Area/PubMed/Corpus">002548</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002548</idno><idno type="wicri:Area/PubMed/Curation">002548</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">002548</idno><idno type="wicri:Area/PubMed/Checkpoint">002277</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">002277</idno><idno type="wicri:Area/Ncbi/Merge">001154</idno><idno type="wicri:Area/Ncbi/Curation">001154</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics.</title><author><name sortKey="Bordi, L" sort="Bordi, L" uniqKey="Bordi L" first="L" last="Bordi">L. 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Piacentini</name></author><author><name sortKey="Capobianchi, M R" sort="Capobianchi, M R" uniqKey="Capobianchi M" first="M R" last="Capobianchi">M R Capobianchi</name></author></analytic><series><title level="j">Archives of virology</title><idno type="ISSN">0304-8608</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Caspases (metabolism)</term><term>Chlorocebus aethiops</term><term>Proto-Oncogene Proteins c-bcl-2 (genetics)</term><term>Proto-Oncogene Proteins c-bcl-2 (metabolism)</term><term>SARS Virus (pathogenicity)</term><term>SARS Virus (physiology)</term><term>Time Factors</term><term>Vero Cells</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Caspases (métabolisme)</term><term>Cellules Vero</term><term>Facteurs temps</term><term>Protéines proto-oncogènes c-bcl-2 (génétique)</term><term>Protéines proto-oncogènes c-bcl-2 (métabolisme)</term><term>Réplication virale</term><term>Virus du SRAS (pathogénicité)</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Proto-Oncogene Proteins c-bcl-2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspases</term><term>Proto-Oncogene Proteins c-bcl-2</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines proto-oncogènes c-bcl-2</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspases</term><term>Protéines proto-oncogènes c-bcl-2</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Chlorocebus aethiops</term><term>Time Factors</term><term>Vero Cells</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Cellules Vero</term><term>Facteurs temps</term><term>Réplication virale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Vero cells transfected with either neo- or bcl-2-plasmid were infected with SARS-CoV at a high multiplicity of infection. Apoptosis appeared after the onset of CPE and completion of virus replication, and could be prevented by Bcl-2 expression. Apoptosis is likely mediated by the mitochondrial pathway, as demonstrated by its inhibition using Bcl-2, and by the activation of the caspase cascade, resulting in PARP cleavage. Prevention of apoptosis did not affect susceptibility to infection, kinetics and extent of viral replication and release, thus implying that apoptosis is not involved in facilitating release and/or dissemination of SARS-CoV in Vero cells.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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