SrasV1, Main, Exploration, bibRecord, 004D67

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

Identifieur interne : 004D67 ( Main/Exploration ); précédent : 004D66; suivant : 004D68

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

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

Source :

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

RBID : Pascal:06-0013783

Descripteurs français

KwdFr :
- Animaux, Cadres ouverts de lecture (génétique), Infections à coronavirus (virologie), Protéines virales (génétique), Protéines virales (physiologie), Protéines virales structurales (génétique), Protéines virales structurales (immunologie), Protéines virales structurales (isolement et purification), Protéines virales structurales (métabolisme), Réplication virale (physiologie), Souris, Virus du SRAS (génétique), Virus du SRAS (pathogénicité), Virus du SRAS (physiologie).
MESH :
- génétique : Cadres ouverts de lecture, Protéines virales, Protéines virales structurales, Virus du SRAS.
- immunologie : Protéines virales structurales.
- isolement et purification : Protéines virales structurales.
- métabolisme : Protéines virales structurales.
- pathogénicité : Virus du SRAS.
- physiologie : Protéines virales, Réplication virale, Virus du SRAS.
- virologie : Infections à coronavirus.
Pascal (Inist)
- Animaux, Coronavirus, Souris, Cadre lecture ouvert, Réplication, Culture cellulaire, Microbiologie, Virologie, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Animals, Cell culture, Coronavirus, Coronavirus Infections (virology), Mice, Microbiology, Mouse, Open Reading Frames (genetics), Open reading frame, Replication, SARS Virus (genetics), SARS Virus (pathogenicity), SARS Virus (physiology), Severe acute respiratory syndrome, Viral Proteins (genetics), Viral Proteins (physiology), Viral Structural Proteins (genetics), Viral Structural Proteins (immunology), Viral Structural Proteins (isolation & purification), Viral Structural Proteins (metabolism), Virology, Virus Replication (physiology).
MESH :
- chemical , genetics : Viral Proteins, Viral Structural Proteins.
- genetics : Open Reading Frames, SARS Virus.
- chemical , immunology : Viral Structural Proteins.
- chemical , isolation & purification : Viral Structural Proteins.
- chemical , metabolism : Viral Structural Proteins.
- pathogenicity : SARS Virus.
- physiology : SARS Virus, Viral Proteins, Virus Replication.
- virology : Coronavirus Infections.
- Animals, Mice.

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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287583

Affiliations:

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Cell culture</term>
<term>Coronavirus</term>
<term>Coronavirus Infections (virology)</term>
<term>Mice</term>
<term>Microbiology</term>
<term>Mouse</term>
<term>Open Reading Frames (genetics)</term>
<term>Open reading frame</term>
<term>Replication</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (pathogenicity)</term>
<term>SARS Virus (physiology)</term>
<term>Severe acute respiratory syndrome</term>
<term>Viral Proteins (genetics)</term>
<term>Viral Proteins (physiology)</term>
<term>Viral Structural Proteins (genetics)</term>
<term>Viral Structural Proteins (immunology)</term>
<term>Viral Structural Proteins (isolation & purification)</term>
<term>Viral Structural Proteins (metabolism)</term>
<term>Virology</term>
<term>Virus Replication (physiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Cadres ouverts de lecture (génétique)</term>
<term>Infections à coronavirus (virologie)</term>
<term>Protéines virales (génétique)</term>
<term>Protéines virales (physiologie)</term>
<term>Protéines virales structurales (génétique)</term>
<term>Protéines virales structurales (immunologie)</term>
<term>Protéines virales structurales (isolement et purification)</term>
<term>Protéines virales structurales (métabolisme)</term>
<term>Réplication virale (physiologie)</term>
<term>Souris</term>
<term>Virus du SRAS (génétique)</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>Viral Proteins</term>
<term>Viral Structural Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Open Reading Frames</term>
<term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cadres ouverts de lecture</term>
<term>Protéines virales</term>
<term>Protéines virales structurales</term>
<term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Protéines virales structurales</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Viral Structural Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="isolation & purification" xml:lang="en"><term>Viral Structural Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr"><term>Protéines virales structurales</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Viral Structural Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines virales structurales</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>Protéines virales</term>
<term>Réplication virale</term>
<term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term>
<term>Viral Proteins</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Coronavirus Infections</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Mice</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Animaux</term>
<term>Coronavirus</term>
<term>Souris</term>
<term>Cadre lecture ouvert</term>
<term>Réplication</term>
<term>Culture cellulaire</term>
<term>Microbiologie</term>
<term>Virologie</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<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>
</front>
</TEI>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Caroline du Nord</li>
<li>Tennessee</li>
</region>
<settlement><li>Chapel Hill (Caroline du Nord)</li>
</settlement>
<orgName><li>Université de Caroline du Nord à Chapel Hill</li>
</orgName>
</list>
<tree><country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Yount, Boyd" sort="Yount, Boyd" uniqKey="Yount B" first="Boyd" last="Yount">Boyd Yount</name>
</region>
<name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S." last="Baric">Ralph S. Baric</name>
<name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S." last="Baric">Ralph S. Baric</name>
<name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S." last="Baric">Ralph S. Baric</name>
<name sortKey="Davis, Nancy" sort="Davis, Nancy" uniqKey="Davis N" first="Nancy" last="Davis">Nancy Davis</name>
<name sortKey="Deming, Damon" sort="Deming, Damon" uniqKey="Deming D" first="Damon" last="Deming">Damon Deming</name>
<name sortKey="Denison, Mark R" sort="Denison, Mark R" uniqKey="Denison M" first="Mark R." last="Denison">Mark R. Denison</name>
<name sortKey="Frieman, Matthew B" sort="Frieman, Matthew B" uniqKey="Frieman M" first="Matthew B." last="Frieman">Matthew B. Frieman</name>
<name sortKey="Roberts, Rhonda S" sort="Roberts, Rhonda S" uniqKey="Roberts R" first="Rhonda S." last="Roberts">Rhonda S. Roberts</name>
<name sortKey="Sims, Amy C" sort="Sims, Amy C" uniqKey="Sims A" first="Amy C." last="Sims">Amy C. Sims</name>
<name sortKey="Sparks, Jennifer" sort="Sparks, Jennifer" uniqKey="Sparks J" first="Jennifer" last="Sparks">Jennifer Sparks</name>
</country>
</tree>
</affiliations>
</record>

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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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