Severe acute respiratory syndrome coronavirus protein 6 accelerates murine hepatitis virus infections by more than one mechanism.
Identifieur interne : 003018 ( Main/Exploration ); précédent : 003017; suivant : 003019Severe acute respiratory syndrome coronavirus protein 6 accelerates murine hepatitis virus infections by more than one mechanism.
Auteurs : Snawar Hussain [États-Unis] ; Stanley Perlman ; Thomas M. GallagherSource :
- Journal of virology [ 1098-5514 ] ; 2008.
Descripteurs français
- KwdFr :
- Caryophérines bêta (antagonistes et inhibiteurs), Extinction de l'expression des gènes, Humains, Infections à coronavirus (virologie), Lignée cellulaire, Petit ARN interférent (génétique), Protéines virales (génétique), Protéines virales (métabolisme), Transport nucléaire actif, Virus de l'hépatite murine (croissance et développement), Virus de l'hépatite murine (physiologie), Virus du SRAS (physiologie).
- MESH :
- antagonistes et inhibiteurs : Caryophérines bêta.
- croissance et développement : Virus de l'hépatite murine.
- génétique : Petit ARN interférent, Protéines virales.
- métabolisme : Protéines virales.
- physiologie : Virus de l'hépatite murine, Virus du SRAS.
- virologie : Infections à coronavirus.
- Extinction de l'expression des gènes, Humains, Lignée cellulaire, Transport nucléaire actif.
English descriptors
- KwdEn :
- Active Transport, Cell Nucleus, Cell Line, Coronavirus Infections (virology), Gene Silencing, Humans, Murine hepatitis virus (growth & development), Murine hepatitis virus (physiology), RNA, Small Interfering (genetics), SARS Virus (physiology), Viral Proteins (genetics), Viral Proteins (metabolism), beta Karyopherins (antagonists & inhibitors).
- MESH :
- chemical , antagonists & inhibitors : beta Karyopherins.
- chemical , genetics : RNA, Small Interfering, Viral Proteins.
- growth & development : Murine hepatitis virus.
- chemical , metabolism : Viral Proteins.
- physiology : Murine hepatitis virus, SARS Virus.
- virology : Coronavirus Infections.
- Active Transport, Cell Nucleus, Cell Line, Gene Silencing, Humans.
Abstract
The severe acute respiratory syndrome coronavirus (SARS-CoV) encodes numerous accessory proteins whose importance in the natural infection process is currently unclear. One of these accessory proteins is set apart by its function in the context of a related murine hepatitis virus (MHV) infection. SARS-CoV protein 6 increases MHV neurovirulence and accelerates MHV infection kinetics in tissue culture. Protein 6 also blocks nuclear import of macromolecules from the cytoplasm, a process known to involve its C-terminal residues interacting with cellular importins. In this study, protein 6 was expressed from plasmid DNAs and accumulated in cells prior to infection by wild-type MHV. Output of MHV progeny was significantly increased by preexisting protein 6. Protein 6 with C-terminal deletion mutations no longer interfered with nuclear import processes but still retained much of the capacity to augment MHV infections. However, some virus growth-enhancing activity could be ascribed to the C-terminal end of protein 6. To determine whether this augmentation provided by the C terminus was derived from interference with nuclear import, we evaluated the virus-modulating effects of small interfering RNAs (siRNAs) directed against importin-beta mRNAs, which down-regulated classical nuclear import pathways. The siRNAs did indeed prime cells for enhanced MHV infection. Our findings indicated that protein 6-mediated nuclear import blocks augmented MHV infections but is clearly not the only way that this accessory protein operates to create a milieu conducive to robust virus growth. Thus, the SARS-CoV protein 6 accelerates MHV infections by more than one mechanism.
DOI: 10.1128/JVI.02406-07
PubMed: 18448520
Affiliations:
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Gallagher</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Active Transport, Cell Nucleus</term><term>Cell Line</term><term>Coronavirus Infections (virology)</term><term>Gene Silencing</term><term>Humans</term><term>Murine hepatitis virus (growth & development)</term><term>Murine hepatitis virus (physiology)</term><term>RNA, Small Interfering (genetics)</term><term>SARS Virus (physiology)</term><term>Viral Proteins (genetics)</term><term>Viral Proteins (metabolism)</term><term>beta Karyopherins (antagonists & inhibitors)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Caryophérines bêta (antagonistes et inhibiteurs)</term><term>Extinction de l'expression des gènes</term><term>Humains</term><term>Infections à coronavirus (virologie)</term><term>Lignée cellulaire</term><term>Petit ARN interférent (génétique)</term><term>Protéines virales (génétique)</term><term>Protéines virales (métabolisme)</term><term>Transport nucléaire actif</term><term>Virus de l'hépatite murine (croissance et développement)</term><term>Virus de l'hépatite murine (physiologie)</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>beta Karyopherins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>RNA, Small Interfering</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Caryophérines bêta</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Virus de l'hépatite murine</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Murine hepatitis virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Petit ARN interférent</term><term>Protéines virales</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Viral Proteins</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines virales</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus de l'hépatite murine</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Murine hepatitis virus</term><term>SARS Virus</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>Active Transport, Cell Nucleus</term><term>Cell Line</term><term>Gene Silencing</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Extinction de l'expression des gènes</term><term>Humains</term><term>Lignée cellulaire</term><term>Transport nucléaire actif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The severe acute respiratory syndrome coronavirus (SARS-CoV) encodes numerous accessory proteins whose importance in the natural infection process is currently unclear. One of these accessory proteins is set apart by its function in the context of a related murine hepatitis virus (MHV) infection. SARS-CoV protein 6 increases MHV neurovirulence and accelerates MHV infection kinetics in tissue culture. Protein 6 also blocks nuclear import of macromolecules from the cytoplasm, a process known to involve its C-terminal residues interacting with cellular importins. In this study, protein 6 was expressed from plasmid DNAs and accumulated in cells prior to infection by wild-type MHV. Output of MHV progeny was significantly increased by preexisting protein 6. Protein 6 with C-terminal deletion mutations no longer interfered with nuclear import processes but still retained much of the capacity to augment MHV infections. However, some virus growth-enhancing activity could be ascribed to the C-terminal end of protein 6. To determine whether this augmentation provided by the C terminus was derived from interference with nuclear import, we evaluated the virus-modulating effects of small interfering RNAs (siRNAs) directed against importin-beta mRNAs, which down-regulated classical nuclear import pathways. The siRNAs did indeed prime cells for enhanced MHV infection. Our findings indicated that protein 6-mediated nuclear import blocks augmented MHV infections but is clearly not the only way that this accessory protein operates to create a milieu conducive to robust virus growth. Thus, the SARS-CoV protein 6 accelerates MHV infections by more than one mechanism.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Illinois</li></region></list><tree><noCountry><name sortKey="Gallagher, Thomas M" sort="Gallagher, Thomas M" uniqKey="Gallagher T" first="Thomas M" last="Gallagher">Thomas M. Gallagher</name><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name></noCountry><country name="États-Unis"><region name="Illinois"><name sortKey="Hussain, Snawar" sort="Hussain, Snawar" uniqKey="Hussain S" first="Snawar" last="Hussain">Snawar Hussain</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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