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 : 000567Severe 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. BaricSource :
- Journal of virology [ 0022-538X ] ; 2005.
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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.
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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:06-0013783Le document en format XML
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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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<fC02 i1="01" i2="X"><s0>002A05C10</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Souris</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Mouse</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Ratón</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Cadre lecture ouvert</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Open reading frame</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Cuadro lectura abierto</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Réplication</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Replication</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Replicación</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Culture cellulaire</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Cell culture</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Cultivo celular</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Microbiologie</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Microbiology</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Microbiología</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Virologie</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Virology</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Virología</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="08" 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>
<fC07 i1="01" i2="X" l="ENG"><s0>Coronaviridae</s0>
<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>
<fC07 i1="03" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Virus</s0>
<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>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0>
<s5>13</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Poumon pathologie</s0>
<s5>16</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21><s1>002</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 06-0013783 INIST</NO>
<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>
<LA>Anglais</LA>
<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>
<CC>002A05C10</CC>
<FD>Coronavirus; Souris; Cadre lecture ouvert; Réplication; Culture cellulaire; Microbiologie; Virologie; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Rodentia; Mammalia; Vertebrata; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie</FG>
<ED>Coronavirus; Mouse; Open reading frame; Replication; Cell culture; Microbiology; Virology; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Rodentia; Mammalia; Vertebrata; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Coronavirus; Ratón; Cuadro lectura abierto; Replicación; Cultivo celular; Microbiología; Virología; Síndrome respiratorio agudo severo</SD>
<LO>INIST-13592.354000135123560450</LO>
<ID>06-0013783</ID>
</server>
</inist>
</record>
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