SrasV1, PascalFrancis, Corpus, bibRecord, 000355

Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis

Identifieur interne : 000355 ( PascalFrancis/Corpus ); précédent : 000354; suivant : 000356

Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis

Auteurs : Chia-Yen Chen ; Yueh-Hsin Ping ; Hsin-Chen Lee ; Kuan-Hsuan Chen ; Yuan-Ming Lee ; Yu-Juin Chan ; Te-Cheng Lien ; Tjin-Shing Jap ; Chi-Hung Lin ; Lung-Sen Kao ; Yi-Ming Arthur Chen

Source :

The Journal of infectious diseases [ 0022-1899 ] ; 2007.

RBID : Pascal:07-0388620

Descripteurs français

Pascal (Inist)
- Homme, Coronavirus, Cadre lecture ouvert, Réplication, Apoptose, Mort cellulaire, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Apoptosis, Cell death, Coronavirus, Human, Open reading frame, Replication, Severe acute respiratory syndrome.

Abstract

Background. A unique genomic difference between human and civet severe acute respiratory syndrome coronaviruses (SARS-CoVs) is that the former has a deletion of 29 nucleotides from open reading frame (orf) 8d that results in the generation of orf8a and orf8b. The objectives of the present study were to analyze antibody reactivity to ORF8a in patients with SARS and to elucidate the function of ORF8a. Methods. Western-blot and immunofluorescent antibody assays were used to detect anti-ORF8a antibody. SARS-CoV HKU39849 was used to infect stable clones expressing ORF8a and cells transfected with small interfering RNA (siRNA). The virus loads (VLs) and cytopathic effects (CPEs) were recorded. Confocal microscopy and several mitochondria-related tests were used to study the function of ORF8a. Results. Two (5.4%) of 37 patients with SARS had anti-ORF8a antibodies. The VLs in the stable clones expressing ORF8a were significantly higher than those in control subjects 5 days after infection. siRNA against orf8a significantly reduced VLs and interrupted the CPE. ORF8a was found to be localized in mitochondria, and overexpression resulted in increases in mitochondrial transmembrane potential, reactive oxygen species production, caspase 3 activity, and cellular apoptosis. Conclusions. ORF8a not only enhances viral replication but also induces apoptosis through a mitochondria-dependent pathway.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A02	`01`			`@0 JIDIAQ`
A03		`1`		`@0 J. infect. dis.`
A05				`@2 196`
A06				`@2 3`
A08	`01`	`1`	`ENG`	`@1 Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis`
A11	`01`	`1`		`@1 CHEN (Chia-Yen)`
A11	`02`	`1`		`@1 PING (Yueh-Hsin)`
A11	`03`	`1`		`@1 LEE (Hsin-Chen)`
A11	`04`	`1`		`@1 CHEN (Kuan-Hsuan)`
A11	`05`	`1`		`@1 LEE (Yuan-Ming)`
A11	`06`	`1`		`@1 CHAN (Yu-Juin)`
A11	`07`	`1`		`@1 LIEN (Te-Cheng)`
A11	`08`	`1`		`@1 JAP (Tjin-Shing)`
A11	`09`	`1`		`@1 LIN (Chi-Hung)`
A11	`10`	`1`		`@1 KAO (Lung-Sen)`
A11	`11`	`1`		`@1 CHEN (Yi-Ming Arthur)`
A14	`01`			`@1 Institute of Public Health, National Yang-Ming University @3 TWN @Z 1 aut. @Z 5 aut. @Z 11 aut.`
A14	`02`			`@1 AIDS Prevention and Research Center, National Yang-Ming University @3 TWN @Z 1 aut. @Z 4 aut. @Z 11 aut.`
A14	`03`			`@1 Institute of Pharmacology, National Yang-Ming University @3 TWN @Z 2 aut. @Z 3 aut.`
A14	`04`			`@1 Division of Clinical Virology, Department of Pathology and Laboratory Medicine @3 TWN @Z 5 aut. @Z 6 aut.`
A14	`05`			`@1 Department of Respiratory Therapy @3 TWN @Z 7 aut.`
A14	`06`			`@1 Section of Biochemistry, Department of Pathology and Laboratory Medicine, Veterans General Hospital @3 TWN @Z 8 aut.`
A14	`07`			`@1 Institute of Microbiology and Immunology, National Yang-Ming University @2 Taipei @3 TWN @Z 9 aut.`
A14	`08`			`@1 Faculty of Life Science, National Yang-Ming University @2 Taipei @3 TWN @Z 10 aut.`
A20				`@1 405-415`
A21				`@1 2007`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 2052 @5 354000146736940090`
A44				`@0 0000 @1 © 2007 INIST-CNRS. All rights reserved.`
A45				`@0 50 ref.`
A47	`01`	`1`		`@0 07-0388620`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 The Journal of infectious diseases`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 Background. A unique genomic difference between human and civet severe acute respiratory syndrome coronaviruses (SARS-CoVs) is that the former has a deletion of 29 nucleotides from open reading frame (orf) 8d that results in the generation of orf8a and orf8b. The objectives of the present study were to analyze antibody reactivity to ORF8a in patients with SARS and to elucidate the function of ORF8a. Methods. Western-blot and immunofluorescent antibody assays were used to detect anti-ORF8a antibody. SARS-CoV HKU39849 was used to infect stable clones expressing ORF8a and cells transfected with small interfering RNA (siRNA). The virus loads (VLs) and cytopathic effects (CPEs) were recorded. Confocal microscopy and several mitochondria-related tests were used to study the function of ORF8a. Results. Two (5.4%) of 37 patients with SARS had anti-ORF8a antibodies. The VLs in the stable clones expressing ORF8a were significantly higher than those in control subjects 5 days after infection. siRNA against orf8a significantly reduced VLs and interrupted the CPE. ORF8a was found to be localized in mitochondria, and overexpression resulted in increases in mitochondrial transmembrane potential, reactive oxygen species production, caspase 3 activity, and cellular apoptosis. Conclusions. ORF8a not only enhances viral replication but also induces apoptosis through a mitochondria-dependent pathway.
C02	`01`	`X`		`@0 002A05C10`
C03	`01`	`X`	`FRE`	`@0 Homme @5 01`
C03	`01`	`X`	`ENG`	`@0 Human @5 01`
C03	`01`	`X`	`SPA`	`@0 Hombre @5 01`
C03	`02`	`X`	`FRE`	`@0 Coronavirus @2 NW @5 02`
C03	`02`	`X`	`ENG`	`@0 Coronavirus @2 NW @5 02`
C03	`02`	`X`	`SPA`	`@0 Coronavirus @2 NW @5 02`
C03	`03`	`X`	`FRE`	`@0 Cadre lecture ouvert @5 05`
C03	`03`	`X`	`ENG`	`@0 Open reading frame @5 05`
C03	`03`	`X`	`SPA`	`@0 Cuadro lectura abierto @5 05`
C03	`04`	`X`	`FRE`	`@0 Réplication @5 06`
C03	`04`	`X`	`ENG`	`@0 Replication @5 06`
C03	`04`	`X`	`SPA`	`@0 Replicación @5 06`
C03	`05`	`X`	`FRE`	`@0 Apoptose @5 07`
C03	`05`	`X`	`ENG`	`@0 Apoptosis @5 07`
C03	`05`	`X`	`SPA`	`@0 Apoptosis @5 07`
C03	`06`	`X`	`FRE`	`@0 Mort cellulaire @5 08`
C03	`06`	`X`	`ENG`	`@0 Cell death @5 08`
C03	`06`	`X`	`SPA`	`@0 Muerte celular @5 08`
C03	`07`	`X`	`FRE`	`@0 Syndrome respiratoire aigu sévère @2 NM @5 14`
C03	`07`	`X`	`ENG`	`@0 Severe acute respiratory syndrome @2 NM @5 14`
C03	`07`	`X`	`SPA`	`@0 Síndrome respiratorio agudo severo @2 NM @5 14`
C07	`01`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`SPA`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`FRE`	`@0 Nidovirales @2 NW`
C07	`02`	`X`	`ENG`	`@0 Nidovirales @2 NW`
C07	`02`	`X`	`SPA`	`@0 Nidovirales @2 NW`
C07	`03`	`X`	`FRE`	`@0 Virus @2 NW`
C07	`03`	`X`	`ENG`	`@0 Virus @2 NW`
C07	`03`	`X`	`SPA`	`@0 Virus @2 NW`
C07	`04`	`X`	`FRE`	`@0 Appareil respiratoire pathologie @5 13`
C07	`04`	`X`	`ENG`	`@0 Respiratory disease @5 13`
C07	`04`	`X`	`SPA`	`@0 Aparato respiratorio patología @5 13`
C07	`05`	`X`	`FRE`	`@0 Virose`
C07	`05`	`X`	`ENG`	`@0 Viral disease`
C07	`05`	`X`	`SPA`	`@0 Virosis`
C07	`06`	`X`	`FRE`	`@0 Infection`
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C07	`06`	`X`	`SPA`	`@0 Infección`
C07	`07`	`X`	`FRE`	`@0 Poumon pathologie @5 16`
C07	`07`	`X`	`ENG`	`@0 Lung disease @5 16`
C07	`07`	`X`	`SPA`	`@0 Pulmón patología @5 16`
N21				`@1 253`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 07-0388620 INIST
ET :	Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis
AU :	CHEN (Chia-Yen); PING (Yueh-Hsin); LEE (Hsin-Chen); CHEN (Kuan-Hsuan); LEE (Yuan-Ming); CHAN (Yu-Juin); LIEN (Te-Cheng); JAP (Tjin-Shing); LIN (Chi-Hung); KAO (Lung-Sen); CHEN (Yi-Ming Arthur)
AF :	Institute of Public Health, National Yang-Ming University/Taïwan (1 aut., 5 aut., 11 aut.); AIDS Prevention and Research Center, National Yang-Ming University/Taïwan (1 aut., 4 aut., 11 aut.); Institute of Pharmacology, National Yang-Ming University/Taïwan (2 aut., 3 aut.); Division of Clinical Virology, Department of Pathology and Laboratory Medicine/Taïwan (5 aut., 6 aut.); Department of Respiratory Therapy/Taïwan (7 aut.); Section of Biochemistry, Department of Pathology and Laboratory Medicine, Veterans General Hospital/Taïwan (8 aut.); Institute of Microbiology and Immunology, National Yang-Ming University/Taipei/Taïwan (9 aut.); Faculty of Life Science, National Yang-Ming University/Taipei/Taïwan (10 aut.)
DT :	Publication en série; Niveau analytique
SO :	The Journal of infectious diseases; ISSN 0022-1899; Coden JIDIAQ; Etats-Unis; Da. 2007; Vol. 196; No. 3; Pp. 405-415; Bibl. 50 ref.
LA :	Anglais
EA :	Background. A unique genomic difference between human and civet severe acute respiratory syndrome coronaviruses (SARS-CoVs) is that the former has a deletion of 29 nucleotides from open reading frame (orf) 8d that results in the generation of orf8a and orf8b. The objectives of the present study were to analyze antibody reactivity to ORF8a in patients with SARS and to elucidate the function of ORF8a. Methods. Western-blot and immunofluorescent antibody assays were used to detect anti-ORF8a antibody. SARS-CoV HKU39849 was used to infect stable clones expressing ORF8a and cells transfected with small interfering RNA (siRNA). The virus loads (VLs) and cytopathic effects (CPEs) were recorded. Confocal microscopy and several mitochondria-related tests were used to study the function of ORF8a. Results. Two (5.4%) of 37 patients with SARS had anti-ORF8a antibodies. The VLs in the stable clones expressing ORF8a were significantly higher than those in control subjects 5 days after infection. siRNA against orf8a significantly reduced VLs and interrupted the CPE. ORF8a was found to be localized in mitochondria, and overexpression resulted in increases in mitochondrial transmembrane potential, reactive oxygen species production, caspase 3 activity, and cellular apoptosis. Conclusions. ORF8a not only enhances viral replication but also induces apoptosis through a mitochondria-dependent pathway.
CC :	002A05C10
FD :	Homme; Coronavirus; Cadre lecture ouvert; Réplication; Apoptose; Mort cellulaire; Syndrome respiratoire aigu sévère
FG :	Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie
ED :	Human; Coronavirus; Open reading frame; Replication; Apoptosis; Cell death; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease
SD :	Hombre; Coronavirus; Cuadro lectura abierto; Replicación; Apoptosis; Muerte celular; Síndrome respiratorio agudo severo
LO :	INIST-2052.354000146736940090
ID :	07-0388620

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Pascal:07-0388620

Le document en format XML

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<author><name sortKey="Chen, Yi Ming Arthur" sort="Chen, Yi Ming Arthur" uniqKey="Chen Y" first="Yi-Ming Arthur" last="Chen">Yi-Ming Arthur Chen</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis</title>
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<author><name sortKey="Lee, Hsin Chen" sort="Lee, Hsin Chen" uniqKey="Lee H" first="Hsin-Chen" last="Lee">Hsin-Chen Lee</name>
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<author><name sortKey="Chen, Kuan Hsuan" sort="Chen, Kuan Hsuan" uniqKey="Chen K" first="Kuan-Hsuan" last="Chen">Kuan-Hsuan Chen</name>
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<author><name sortKey="Lee, Yuan Ming" sort="Lee, Yuan Ming" uniqKey="Lee Y" first="Yuan-Ming" last="Lee">Yuan-Ming Lee</name>
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<s3>TWN</s3>
<sZ>1 aut.</sZ>
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<affiliation><inist:fA14 i1="04"><s1>Division of Clinical Virology, Department of Pathology and Laboratory Medicine</s1>
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<author><name sortKey="Chan, Yu Juin" sort="Chan, Yu Juin" uniqKey="Chan Y" first="Yu-Juin" last="Chan">Yu-Juin Chan</name>
<affiliation><inist:fA14 i1="04"><s1>Division of Clinical Virology, Department of Pathology and Laboratory Medicine</s1>
<s3>TWN</s3>
<sZ>5 aut.</sZ>
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<author><name sortKey="Lien, Te Cheng" sort="Lien, Te Cheng" uniqKey="Lien T" first="Te-Cheng" last="Lien">Te-Cheng Lien</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Respiratory Therapy</s1>
<s3>TWN</s3>
<sZ>7 aut.</sZ>
</inist:fA14>
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<author><name sortKey="Jap, Tjin Shing" sort="Jap, Tjin Shing" uniqKey="Jap T" first="Tjin-Shing" last="Jap">Tjin-Shing Jap</name>
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<s3>TWN</s3>
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<author><name sortKey="Lin, Chi Hung" sort="Lin, Chi Hung" uniqKey="Lin C" first="Chi-Hung" last="Lin">Chi-Hung Lin</name>
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<s2>Taipei</s2>
<s3>TWN</s3>
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</author>
<author><name sortKey="Kao, Lung Sen" sort="Kao, Lung Sen" uniqKey="Kao L" first="Lung-Sen" last="Kao">Lung-Sen Kao</name>
<affiliation><inist:fA14 i1="08"><s1>Faculty of Life Science, National Yang-Ming University</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
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</author>
<author><name sortKey="Chen, Yi Ming Arthur" sort="Chen, Yi Ming Arthur" uniqKey="Chen Y" first="Yi-Ming Arthur" last="Chen">Yi-Ming Arthur Chen</name>
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<series><title level="j" type="main">The Journal of infectious diseases</title>
<title level="j" type="abbreviated">J. infect. dis.</title>
<idno type="ISSN">0022-1899</idno>
<imprint><date when="2007">2007</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">The Journal of infectious diseases</title>
<title level="j" type="abbreviated">J. infect. dis.</title>
<idno type="ISSN">0022-1899</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term>
<term>Cell death</term>
<term>Coronavirus</term>
<term>Human</term>
<term>Open reading frame</term>
<term>Replication</term>
<term>Severe acute respiratory syndrome</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Homme</term>
<term>Coronavirus</term>
<term>Cadre lecture ouvert</term>
<term>Réplication</term>
<term>Apoptose</term>
<term>Mort cellulaire</term>
<term>Syndrome respiratoire aigu sévère</term>
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<front><div type="abstract" xml:lang="en">Background. A unique genomic difference between human and civet severe acute respiratory syndrome coronaviruses (SARS-CoVs) is that the former has a deletion of 29 nucleotides from open reading frame (orf) 8d that results in the generation of orf8a and orf8b. The objectives of the present study were to analyze antibody reactivity to ORF8a in patients with SARS and to elucidate the function of ORF8a. Methods. Western-blot and immunofluorescent antibody assays were used to detect anti-ORF8a antibody. SARS-CoV HKU39849 was used to infect stable clones expressing ORF8a and cells transfected with small interfering RNA (siRNA). The virus loads (VLs) and cytopathic effects (CPEs) were recorded. Confocal microscopy and several mitochondria-related tests were used to study the function of ORF8a. Results. Two (5.4%) of 37 patients with SARS had anti-ORF8a antibodies. The VLs in the stable clones expressing ORF8a were significantly higher than those in control subjects 5 days after infection. siRNA against orf8a significantly reduced VLs and interrupted the CPE. ORF8a was found to be localized in mitochondria, and overexpression resulted in increases in mitochondrial transmembrane potential, reactive oxygen species production, caspase 3 activity, and cellular apoptosis. Conclusions. ORF8a not only enhances viral replication but also induces apoptosis through a mitochondria-dependent pathway.</div>
</front>
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<fA02 i1="01"><s0>JIDIAQ</s0>
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<fA03 i2="1"><s0>J. infect. dis.</s0>
</fA03>
<fA05><s2>196</s2>
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<fA06><s2>3</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>CHEN (Chia-Yen)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>PING (Yueh-Hsin)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>LEE (Hsin-Chen)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>CHEN (Kuan-Hsuan)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>LEE (Yuan-Ming)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>CHAN (Yu-Juin)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>LIEN (Te-Cheng)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>JAP (Tjin-Shing)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>LIN (Chi-Hung)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>KAO (Lung-Sen)</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>CHEN (Yi-Ming Arthur)</s1>
</fA11>
<fA14 i1="01"><s1>Institute of Public Health, National Yang-Ming University</s1>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>AIDS Prevention and Research Center, National Yang-Ming University</s1>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Institute of Pharmacology, National Yang-Ming University</s1>
<s3>TWN</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Division of Clinical Virology, Department of Pathology and Laboratory Medicine</s1>
<s3>TWN</s3>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Respiratory Therapy</s1>
<s3>TWN</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Section of Biochemistry, Department of Pathology and Laboratory Medicine, Veterans General Hospital</s1>
<s3>TWN</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Institute of Microbiology and Immunology, National Yang-Ming University</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>Faculty of Life Science, National Yang-Ming University</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA20><s1>405-415</s1>
</fA20>
<fA21><s1>2007</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>2052</s2>
<s5>354000146736940090</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2007 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>50 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>07-0388620</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>The Journal of infectious diseases</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Background. A unique genomic difference between human and civet severe acute respiratory syndrome coronaviruses (SARS-CoVs) is that the former has a deletion of 29 nucleotides from open reading frame (orf) 8d that results in the generation of orf8a and orf8b. The objectives of the present study were to analyze antibody reactivity to ORF8a in patients with SARS and to elucidate the function of ORF8a. Methods. Western-blot and immunofluorescent antibody assays were used to detect anti-ORF8a antibody. SARS-CoV HKU39849 was used to infect stable clones expressing ORF8a and cells transfected with small interfering RNA (siRNA). The virus loads (VLs) and cytopathic effects (CPEs) were recorded. Confocal microscopy and several mitochondria-related tests were used to study the function of ORF8a. Results. Two (5.4%) of 37 patients with SARS had anti-ORF8a antibodies. The VLs in the stable clones expressing ORF8a were significantly higher than those in control subjects 5 days after infection. siRNA against orf8a significantly reduced VLs and interrupted the CPE. ORF8a was found to be localized in mitochondria, and overexpression resulted in increases in mitochondrial transmembrane potential, reactive oxygen species production, caspase 3 activity, and cellular apoptosis. Conclusions. ORF8a not only enhances viral replication but also induces apoptosis through a mitochondria-dependent pathway.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A05C10</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Homme</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Human</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Hombre</s0>
<s5>01</s5>
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<s5>02</s5>
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<fC03 i1="02" i2="X" l="ENG"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>02</s5>
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<fC03 i1="02" i2="X" l="SPA"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>02</s5>
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<fC03 i1="03" i2="X" l="FRE"><s0>Cadre lecture ouvert</s0>
<s5>05</s5>
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<s5>05</s5>
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<fC03 i1="03" i2="X" l="SPA"><s0>Cuadro lectura abierto</s0>
<s5>05</s5>
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<fC03 i1="04" i2="X" l="FRE"><s0>Réplication</s0>
<s5>06</s5>
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<fC03 i1="04" i2="X" l="ENG"><s0>Replication</s0>
<s5>06</s5>
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<fC03 i1="04" i2="X" l="SPA"><s0>Replicación</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Apoptose</s0>
<s5>07</s5>
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<fC03 i1="05" i2="X" l="ENG"><s0>Apoptosis</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Apoptosis</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Mort cellulaire</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Cell death</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Muerte celular</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
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<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
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<s2>NW</s2>
</fC07>
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<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0>
<s5>13</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Poumon pathologie</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21><s1>253</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
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<server><NO>PASCAL 07-0388620 INIST</NO>
<ET>Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis</ET>
<AU>CHEN (Chia-Yen); PING (Yueh-Hsin); LEE (Hsin-Chen); CHEN (Kuan-Hsuan); LEE (Yuan-Ming); CHAN (Yu-Juin); LIEN (Te-Cheng); JAP (Tjin-Shing); LIN (Chi-Hung); KAO (Lung-Sen); CHEN (Yi-Ming Arthur)</AU>
<AF>Institute of Public Health, National Yang-Ming University/Taïwan (1 aut., 5 aut., 11 aut.); AIDS Prevention and Research Center, National Yang-Ming University/Taïwan (1 aut., 4 aut., 11 aut.); Institute of Pharmacology, National Yang-Ming University/Taïwan (2 aut., 3 aut.); Division of Clinical Virology, Department of Pathology and Laboratory Medicine/Taïwan (5 aut., 6 aut.); Department of Respiratory Therapy/Taïwan (7 aut.); Section of Biochemistry, Department of Pathology and Laboratory Medicine, Veterans General Hospital/Taïwan (8 aut.); Institute of Microbiology and Immunology, National Yang-Ming University/Taipei/Taïwan (9 aut.); Faculty of Life Science, National Yang-Ming University/Taipei/Taïwan (10 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>The Journal of infectious diseases; ISSN 0022-1899; Coden JIDIAQ; Etats-Unis; Da. 2007; Vol. 196; No. 3; Pp. 405-415; Bibl. 50 ref.</SO>
<LA>Anglais</LA>
<EA>Background. A unique genomic difference between human and civet severe acute respiratory syndrome coronaviruses (SARS-CoVs) is that the former has a deletion of 29 nucleotides from open reading frame (orf) 8d that results in the generation of orf8a and orf8b. The objectives of the present study were to analyze antibody reactivity to ORF8a in patients with SARS and to elucidate the function of ORF8a. Methods. Western-blot and immunofluorescent antibody assays were used to detect anti-ORF8a antibody. SARS-CoV HKU39849 was used to infect stable clones expressing ORF8a and cells transfected with small interfering RNA (siRNA). The virus loads (VLs) and cytopathic effects (CPEs) were recorded. Confocal microscopy and several mitochondria-related tests were used to study the function of ORF8a. Results. Two (5.4%) of 37 patients with SARS had anti-ORF8a antibodies. The VLs in the stable clones expressing ORF8a were significantly higher than those in control subjects 5 days after infection. siRNA against orf8a significantly reduced VLs and interrupted the CPE. ORF8a was found to be localized in mitochondria, and overexpression resulted in increases in mitochondrial transmembrane potential, reactive oxygen species production, caspase 3 activity, and cellular apoptosis. Conclusions. ORF8a not only enhances viral replication but also induces apoptosis through a mitochondria-dependent pathway.</EA>
<CC>002A05C10</CC>
<FD>Homme; Coronavirus; Cadre lecture ouvert; Réplication; Apoptose; Mort cellulaire; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie</FG>
<ED>Human; Coronavirus; Open reading frame; Replication; Apoptosis; Cell death; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Hombre; Coronavirus; Cuadro lectura abierto; Replicación; Apoptosis; Muerte celular; Síndrome respiratorio agudo severo</SD>
<LO>INIST-2052.354000146736940090</LO>
<ID>07-0388620</ID>
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Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis

Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis

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