SrasV1, PascalFrancis, Corpus, bibRecord, 000566

Severe acute respiratory syndrome coronavirus group-specific open reading frames encode nonessential functions for replication in cell cultures and mice

Identifieur interne : 000566 ( PascalFrancis/Corpus ); précédent : 000565; suivant : 000567

Severe acute respiratory syndrome coronavirus group-specific open reading frames encode nonessential functions for replication in cell cultures and mice

Auteurs : Boyd Yount ; Rhonda S. Roberts ; Amy C. Sims ; Damon Deming ; Matthew B. Frieman ; Jennifer Sparks ; Mark R. Denison ; Nancy Davis ; Ralph S. Baric

Source :

Journal of virology [ 0022-538X ] ; 2005.

RBID : Pascal:06-0013783

Descripteurs français

Pascal (Inist)
- Coronavirus, Souris, Cadre lecture ouvert, Réplication, Culture cellulaire, Microbiologie, Virologie, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Cell culture, Coronavirus, Microbiology, Mouse, Open reading frame, Replication, Severe acute respiratory syndrome, Virology.

Abstract

SARS coronavirus (SARS-CoV) encodes several unique group-specific open reading frames (ORFs) relative to other known coronaviruses. To determine the significance of the SARS-CoV group-specific ORFs in virus replication in vitro and in mice, we systematically deleted five of the eight group-specific ORFs, ORF3a, OF3b, ORF6, ORF7a, and ORF7b, and characterized recombinant virus replication and gene expression in vitro. Deletion of the group-specific ORFs of SARS-CoV, either alone or in various combinations, did not dramatically influence replication efficiency in cell culture or in the levels of viral RNA synthesis. The greatest reduction in virus growth was noted following ORF3a deletion. SARS-CoV spike (S) glycoprotein does not encode a rough endoplasmic reticulum (rER)/Golgi retention signal, and it has been suggested that ORF3a interacts with and targets S glycoprotein retention in the rER/Golgi apparatus. Deletion of ORF3a did not alter subcellular localization of the S glycoprotein from distinct punctuate localization in the rER/Golgi apparatus. These data suggest that ORF3a plays little role in the targeting of S localization in the rER/Golgi apparatus. In addition, insertion of the 29-bp deletion fusing ORF8a/b into the single ORF8, noted in early-stage SARS-CoV human and civet cat isolates, had little if any impact on in vitro growth or RNA synthesis. All recombinant viruses replicated to wild-type levels in the murine model, suggesting that either the group-specific ORFs play little role in in vivo replication efficiency or that the mouse model is not of sufficient quality for discerning the role of the group-specific ORFs in disease origin and development.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 06-0013783 INIST
ET :	Severe acute respiratory syndrome coronavirus group-specific open reading frames encode nonessential functions for replication in cell cultures and mice
AU :	YOUNT (Boyd); ROBERTS (Rhonda S.); SIMS (Amy C.); DEMING (Damon); FRIEMAN (Matthew B.); SPARKS (Jennifer); DENISON (Mark R.); DAVIS (Nancy); BARIC (Ralph S.)
AF :	Department of Epidemiology, School of Public Health, University of North Carolina at Chapel Hill/Chapel Hill, North Carolina 27599-7435/Etats-Unis (1 aut., 2 aut., 3 aut., 5 aut., 9 aut.); Department of Microbiology and Immunology, School of Medicine, University of North Carolina at Chapel Hill/Chapel Hill, North Carolina 27599-7290/Etats-Unis (4 aut., 9 aut.); Department of Microbiology and Immunology and Department of Pediatrics, Vanderbilt University/Nashville, Tennessee/Etats-Unis (6 aut., 7 aut.); Carolina Vaccine Institute, School of Medicine, University of North Carolina at Chapel Hill/Chapel Hill, North Carolina 27599-7290/Etats-Unis (8 aut., 9 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2005; Vol. 79; No. 23; Pp. 14909-14922; Bibl. 75 ref.
LA :	Anglais
EA :	SARS coronavirus (SARS-CoV) encodes several unique group-specific open reading frames (ORFs) relative to other known coronaviruses. To determine the significance of the SARS-CoV group-specific ORFs in virus replication in vitro and in mice, we systematically deleted five of the eight group-specific ORFs, ORF3a, OF3b, ORF6, ORF7a, and ORF7b, and characterized recombinant virus replication and gene expression in vitro. Deletion of the group-specific ORFs of SARS-CoV, either alone or in various combinations, did not dramatically influence replication efficiency in cell culture or in the levels of viral RNA synthesis. The greatest reduction in virus growth was noted following ORF3a deletion. SARS-CoV spike (S) glycoprotein does not encode a rough endoplasmic reticulum (rER)/Golgi retention signal, and it has been suggested that ORF3a interacts with and targets S glycoprotein retention in the rER/Golgi apparatus. Deletion of ORF3a did not alter subcellular localization of the S glycoprotein from distinct punctuate localization in the rER/Golgi apparatus. These data suggest that ORF3a plays little role in the targeting of S localization in the rER/Golgi apparatus. In addition, insertion of the 29-bp deletion fusing ORF8a/b into the single ORF8, noted in early-stage SARS-CoV human and civet cat isolates, had little if any impact on in vitro growth or RNA synthesis. All recombinant viruses replicated to wild-type levels in the murine model, suggesting that either the group-specific ORFs play little role in in vivo replication efficiency or that the mouse model is not of sufficient quality for discerning the role of the group-specific ORFs in disease origin and development.
CC :	002A05C10
FD :	Coronavirus; Souris; Cadre lecture ouvert; Réplication; Culture cellulaire; Microbiologie; Virologie; Syndrome respiratoire aigu sévère
FG :	Coronaviridae; Nidovirales; Virus; Rodentia; Mammalia; Vertebrata; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie
ED :	Coronavirus; Mouse; Open reading frame; Replication; Cell culture; Microbiology; Virology; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Rodentia; Mammalia; Vertebrata; Respiratory disease; Viral disease; Infection; Lung disease
SD :	Coronavirus; Ratón; Cuadro lectura abierto; Replicación; Cultivo celular; Microbiología; Virología; Síndrome respiratorio agudo severo
LO :	INIST-13592.354000135123560450
ID :	06-0013783

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Pascal:06-0013783

Le document en format XML

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<author><name sortKey="Davis, Nancy" sort="Davis, Nancy" uniqKey="Davis N" first="Nancy" last="Davis">Nancy Davis</name>
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<front><div type="abstract" xml:lang="en">SARS coronavirus (SARS-CoV) encodes several unique group-specific open reading frames (ORFs) relative to other known coronaviruses. To determine the significance of the SARS-CoV group-specific ORFs in virus replication in vitro and in mice, we systematically deleted five of the eight group-specific ORFs, ORF3a, OF3b, ORF6, ORF7a, and ORF7b, and characterized recombinant virus replication and gene expression in vitro. Deletion of the group-specific ORFs of SARS-CoV, either alone or in various combinations, did not dramatically influence replication efficiency in cell culture or in the levels of viral RNA synthesis. The greatest reduction in virus growth was noted following ORF3a deletion. SARS-CoV spike (S) glycoprotein does not encode a rough endoplasmic reticulum (rER)/Golgi retention signal, and it has been suggested that ORF3a interacts with and targets S glycoprotein retention in the rER/Golgi apparatus. Deletion of ORF3a did not alter subcellular localization of the S glycoprotein from distinct punctuate localization in the rER/Golgi apparatus. These data suggest that ORF3a plays little role in the targeting of S localization in the rER/Golgi apparatus. In addition, insertion of the 29-bp deletion fusing ORF8a/b into the single ORF8, noted in early-stage SARS-CoV human and civet cat isolates, had little if any impact on in vitro growth or RNA synthesis. All recombinant viruses replicated to wild-type levels in the murine model, suggesting that either the group-specific ORFs play little role in in vivo replication efficiency or that the mouse model is not of sufficient quality for discerning the role of the group-specific ORFs in disease origin and development.</div>
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<ET>Severe acute respiratory syndrome coronavirus group-specific open reading frames encode nonessential functions for replication in cell cultures and mice</ET>
<AU>YOUNT (Boyd); ROBERTS (Rhonda S.); SIMS (Amy C.); DEMING (Damon); FRIEMAN (Matthew B.); SPARKS (Jennifer); DENISON (Mark R.); DAVIS (Nancy); BARIC (Ralph S.)</AU>
<AF>Department of Epidemiology, School of Public Health, University of North Carolina at Chapel Hill/Chapel Hill, North Carolina 27599-7435/Etats-Unis (1 aut., 2 aut., 3 aut., 5 aut., 9 aut.); Department of Microbiology and Immunology, School of Medicine, University of North Carolina at Chapel Hill/Chapel Hill, North Carolina 27599-7290/Etats-Unis (4 aut., 9 aut.); Department of Microbiology and Immunology and Department of Pediatrics, Vanderbilt University/Nashville, Tennessee/Etats-Unis (6 aut., 7 aut.); Carolina Vaccine Institute, School of Medicine, University of North Carolina at Chapel Hill/Chapel Hill, North Carolina 27599-7290/Etats-Unis (8 aut., 9 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2005; Vol. 79; No. 23; Pp. 14909-14922; Bibl. 75 ref.</SO>
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<EA>SARS coronavirus (SARS-CoV) encodes several unique group-specific open reading frames (ORFs) relative to other known coronaviruses. To determine the significance of the SARS-CoV group-specific ORFs in virus replication in vitro and in mice, we systematically deleted five of the eight group-specific ORFs, ORF3a, OF3b, ORF6, ORF7a, and ORF7b, and characterized recombinant virus replication and gene expression in vitro. Deletion of the group-specific ORFs of SARS-CoV, either alone or in various combinations, did not dramatically influence replication efficiency in cell culture or in the levels of viral RNA synthesis. The greatest reduction in virus growth was noted following ORF3a deletion. SARS-CoV spike (S) glycoprotein does not encode a rough endoplasmic reticulum (rER)/Golgi retention signal, and it has been suggested that ORF3a interacts with and targets S glycoprotein retention in the rER/Golgi apparatus. Deletion of ORF3a did not alter subcellular localization of the S glycoprotein from distinct punctuate localization in the rER/Golgi apparatus. These data suggest that ORF3a plays little role in the targeting of S localization in the rER/Golgi apparatus. In addition, insertion of the 29-bp deletion fusing ORF8a/b into the single ORF8, noted in early-stage SARS-CoV human and civet cat isolates, had little if any impact on in vitro growth or RNA synthesis. All recombinant viruses replicated to wild-type levels in the murine model, suggesting that either the group-specific ORFs play little role in in vivo replication efficiency or that the mouse model is not of sufficient quality for discerning the role of the group-specific ORFs in disease origin and development.</EA>
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<ED>Coronavirus; Mouse; Open reading frame; Replication; Cell culture; Microbiology; Virology; Severe acute respiratory syndrome</ED>
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Severe acute respiratory syndrome coronavirus group-specific open reading frames encode nonessential functions for replication in cell cultures and mice

Severe acute respiratory syndrome coronavirus group-specific open reading frames encode nonessential functions for replication in cell cultures and mice

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