SrasV1, PascalFrancis, Corpus, bibRecord, 000500

Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics

Identifieur interne : 000500 ( PascalFrancis/Corpus ); précédent : 000499; suivant : 000501

Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics

Auteurs : L. Bordi ; C. Castilletti ; L. Falasca ; F. Ciccosanti ; S. Calcaterra ; G. Rozera ; A. Di Caro ; S. Zaniratti ; A. Rinaldi ; G. Ippolito ; M. Piacentini ; M. R. Capobianchi

Source :

Archives of virology [ 0304-8608 ] ; 2006.

RBID : Pascal:06-0257128

Descripteurs français

Pascal (Inist)
- Virus syndrome respiratoire aigu sévère, Caspase, Apoptose, Mort cellulaire, Réplication, Cinétique.

English descriptors

KwdEn :
- Apoptosis, Caspase, Cell death, Kinetics, Replication, Severe acute respiratory syndrome virus.

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`06`	`1`		`@1 ROZERA (G.)`
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A11	`08`	`1`		`@1 ZANIRATTI (S.)`
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A11	`12`	`1`		`@1 CAPOBIANCHI (M. R.)`
A14	`01`			`@1 Laboratory of Virology, National Institute for Infectious Diseases INMI "L. Spallanzani" @2 Rome @3 ITA @Z 1 aut. @Z 2 aut. @Z 5 aut. @Z 6 aut. @Z 7 aut. @Z 8 aut. @Z 12 aut.`
A14	`02`			`@1 Laboratory of Cell Biology and Electron Microscopy, National Institute for Infectious Diseases INMI "L. Spallanzani" @2 Rome @3 ITA @Z 3 aut. @Z 4 aut. @Z 9 aut. @Z 11 aut.`
A14	`03`			`@1 Department of Epidemiology, National Institute for Infectious Diseases INMI "L. Spallanzani" @2 Rome @3 ITA @Z 10 aut.`
A14	`04`			`@1 Department of Biology, University of Rome "Tor Vergata" @2 Rome @3 ITA @Z 11 aut.`
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A64	`01`	`1`		`@0 Archives of virology`
A66	`01`			`@0 AUT`
C01	`01`		`ENG`	@0 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.
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C07	`01`	`X`	`ENG`	`@0 Coronavirus @2 NW`
C07	`01`	`X`	`SPA`	`@0 Coronavirus @2 NW`
C07	`02`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`SPA`	`@0 Coronaviridae @2 NW`
C07	`03`	`X`	`FRE`	`@0 Nidovirales @2 NW`
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N21				`@1 163`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 06-0257128 INIST
ET :	Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics
AU :	BORDI (L.); CASTILLETTI (C.); FALASCA (L.); CICCOSANTI (F.); CALCATERRA (S.); ROZERA (G.); DI CARO (A.); ZANIRATTI (S.); RINALDI (A.); IPPOLITO (G.); PIACENTINI (M.); CAPOBIANCHI (M. R.)
AF :	Laboratory of Virology, National Institute for Infectious Diseases INMI "L. Spallanzani"/Rome/Italie (1 aut., 2 aut., 5 aut., 6 aut., 7 aut., 8 aut., 12 aut.); Laboratory of Cell Biology and Electron Microscopy, National Institute for Infectious Diseases INMI "L. Spallanzani"/Rome/Italie (3 aut., 4 aut., 9 aut., 11 aut.); Department of Epidemiology, National Institute for Infectious Diseases INMI "L. Spallanzani"/Rome/Italie (10 aut.); Department of Biology, University of Rome "Tor Vergata"/Rome/Italie (11 aut.)
DT :	Publication en série; Courte communication, note brève; Niveau analytique
SO :	Archives of virology; ISSN 0304-8608; Autriche; Da. 2006; Vol. 151; No. 2; Pp. 369-377; Bibl. 27 ref.
LA :	Anglais
EA :	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.
CC :	002A05C10
FD :	Virus syndrome respiratoire aigu sévère; Caspase; Apoptose; Mort cellulaire; Réplication; Cinétique
FG :	Coronavirus; Coronaviridae; Nidovirales; Virus; Peptidases; Hydrolases; Enzyme
ED :	Severe acute respiratory syndrome virus; Caspase; Apoptosis; Cell death; Replication; Kinetics
EG :	Coronavirus; Coronaviridae; Nidovirales; Virus; Peptidases; Hydrolases; Enzyme
SD :	Severe acute respiratory syndrome virus; Caspase; Apoptosis; Muerte celular; Replicación; Cinética
LO :	INIST-6355.354000135727800130
ID :	06-0257128

Links to Exploration step

Pascal:06-0257128

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics</title>
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<author><name sortKey="Rozera, G" sort="Rozera, G" uniqKey="Rozera G" first="G." last="Rozera">G. Rozera</name>
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<author><name sortKey="Di Caro, A" sort="Di Caro, A" uniqKey="Di Caro A" first="A." last="Di Caro">A. Di Caro</name>
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<author><name sortKey="Zaniratti, S" sort="Zaniratti, S" uniqKey="Zaniratti S" first="S." last="Zaniratti">S. Zaniratti</name>
<affiliation><inist:fA14 i1="01"><s1>Laboratory of Virology, National Institute for Infectious Diseases INMI "L. Spallanzani"</s1>
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<author><name sortKey="Rinaldi, A" sort="Rinaldi, A" uniqKey="Rinaldi A" first="A." last="Rinaldi">A. Rinaldi</name>
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<author><name sortKey="Ippolito, G" sort="Ippolito, G" uniqKey="Ippolito G" first="G." last="Ippolito">G. Ippolito</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Epidemiology, National Institute for Infectious Diseases INMI "L. Spallanzani"</s1>
<s2>Rome</s2>
<s3>ITA</s3>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Piacentini, M" sort="Piacentini, M" uniqKey="Piacentini M" first="M." last="Piacentini">M. Piacentini</name>
<affiliation><inist:fA14 i1="02"><s1>Laboratory of Cell Biology and Electron Microscopy, National Institute for Infectious Diseases INMI "L. Spallanzani"</s1>
<s2>Rome</s2>
<s3>ITA</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="04"><s1>Department of Biology, University of Rome "Tor Vergata"</s1>
<s2>Rome</s2>
<s3>ITA</s3>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Capobianchi, M R" sort="Capobianchi, M R" uniqKey="Capobianchi M" first="M. R." last="Capobianchi">M. R. Capobianchi</name>
<affiliation><inist:fA14 i1="01"><s1>Laboratory of Virology, National Institute for Infectious Diseases INMI "L. Spallanzani"</s1>
<s2>Rome</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>12 aut.</sZ>
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<series><title level="j" type="main">Archives of virology</title>
<title level="j" type="abbreviated">Arch. virol.</title>
<idno type="ISSN">0304-8608</idno>
<imprint><date when="2006">2006</date>
</imprint>
</series>
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<seriesStmt><title level="j" type="main">Archives of virology</title>
<title level="j" type="abbreviated">Arch. virol.</title>
<idno type="ISSN">0304-8608</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term>
<term>Caspase</term>
<term>Cell death</term>
<term>Kinetics</term>
<term>Replication</term>
<term>Severe acute respiratory syndrome virus</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Virus syndrome respiratoire aigu sévère</term>
<term>Caspase</term>
<term>Apoptose</term>
<term>Mort cellulaire</term>
<term>Réplication</term>
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<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>
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<fA14 i1="01"><s1>Laboratory of Virology, National Institute for Infectious Diseases INMI "L. Spallanzani"</s1>
<s2>Rome</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
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<sZ>8 aut.</sZ>
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<fA14 i1="02"><s1>Laboratory of Cell Biology and Electron Microscopy, National Institute for Infectious Diseases INMI "L. Spallanzani"</s1>
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<s3>ITA</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Epidemiology, National Institute for Infectious Diseases INMI "L. Spallanzani"</s1>
<s2>Rome</s2>
<s3>ITA</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Biology, University of Rome "Tor Vergata"</s1>
<s2>Rome</s2>
<s3>ITA</s3>
<sZ>11 aut.</sZ>
</fA14>
<fA20><s1>369-377</s1>
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<fC01 i1="01" l="ENG"><s0>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.</s0>
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<s2>NW</s2>
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<fC07 i1="07" i2="X" l="SPA"><s0>Enzima</s0>
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<server><NO>PASCAL 06-0257128 INIST</NO>
<ET>Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics</ET>
<AU>BORDI (L.); CASTILLETTI (C.); FALASCA (L.); CICCOSANTI (F.); CALCATERRA (S.); ROZERA (G.); DI CARO (A.); ZANIRATTI (S.); RINALDI (A.); IPPOLITO (G.); PIACENTINI (M.); CAPOBIANCHI (M. R.)</AU>
<AF>Laboratory of Virology, National Institute for Infectious Diseases INMI "L. Spallanzani"/Rome/Italie (1 aut., 2 aut., 5 aut., 6 aut., 7 aut., 8 aut., 12 aut.); Laboratory of Cell Biology and Electron Microscopy, National Institute for Infectious Diseases INMI "L. Spallanzani"/Rome/Italie (3 aut., 4 aut., 9 aut., 11 aut.); Department of Epidemiology, National Institute for Infectious Diseases INMI "L. Spallanzani"/Rome/Italie (10 aut.); Department of Biology, University of Rome "Tor Vergata"/Rome/Italie (11 aut.)</AF>
<DT>Publication en série; Courte communication, note brève; Niveau analytique</DT>
<SO>Archives of virology; ISSN 0304-8608; Autriche; Da. 2006; Vol. 151; No. 2; Pp. 369-377; Bibl. 27 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002A05C10</CC>
<FD>Virus syndrome respiratoire aigu sévère; Caspase; Apoptose; Mort cellulaire; Réplication; Cinétique</FD>
<FG>Coronavirus; Coronaviridae; Nidovirales; Virus; Peptidases; Hydrolases; Enzyme</FG>
<ED>Severe acute respiratory syndrome virus; Caspase; Apoptosis; Cell death; Replication; Kinetics</ED>
<EG>Coronavirus; Coronaviridae; Nidovirales; Virus; Peptidases; Hydrolases; Enzyme</EG>
<SD>Severe acute respiratory syndrome virus; Caspase; Apoptosis; Muerte celular; Replicación; Cinética</SD>
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<ID>06-0257128</ID>
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Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics

Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics

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