Severe Acute Respiratory Syndrome Coronavirus Protein 6 Accelerates Murine Hepatitis Virus Infections by More than One Mechanism
Identifieur interne : 003472 ( Main/Exploration ); précédent : 003471; suivant : 003473Severe Acute Respiratory Syndrome Coronavirus Protein 6 Accelerates Murine Hepatitis Virus Infections by More than One Mechanism
Auteurs : Snawar Hussain [États-Unis] ; Stanley Perlman [États-Unis] ; Thomas M. Gallagher [États-Unis]Source :
- Journal of virology [ 0022-538X ] ; 2008.
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- Pascal (Inist)
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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-p 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.
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Gallagher</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, Loyola University Medical Center</s1><s2>Maywood, Illinois</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Illinois</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">08-0351234</idno><date when="2008">2008</date><idno type="stanalyst">PASCAL 08-0351234 INIST</idno><idno type="RBID">Pascal:08-0351234</idno><idno type="wicri:Area/PascalFrancis/Corpus">000267</idno><idno type="wicri:Area/PascalFrancis/Curation">000721</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000252</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000252</idno><idno type="wicri:doubleKey">0022-538X:2008:Hussain S:severe:acute:respiratory</idno><idno type="wicri:Area/Main/Merge">003578</idno><idno type="wicri:Area/Main/Curation">003472</idno><idno type="wicri:Area/Main/Exploration">003472</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Severe Acute Respiratory Syndrome Coronavirus Protein 6 Accelerates Murine Hepatitis Virus Infections by More than One Mechanism</title><author><name sortKey="Hussain, Snawar" sort="Hussain, Snawar" uniqKey="Hussain S" first="Snawar" last="Hussain">Snawar Hussain</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, Loyola University Medical Center</s1><s2>Maywood, Illinois</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Illinois</region></placeName></affiliation></author><author><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Interdisciplinary Program in Immunology, Department of Microbiology, University of Iowa</s1><s2>Iowa City, Iowa</s2><s3>USA</s3><sZ>2 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Iowa</region><settlement type="city">Iowa City</settlement></placeName><orgName type="university">Université de l'Iowa</orgName></affiliation></author><author><name sortKey="Gallagher, Thomas M" sort="Gallagher, Thomas M" uniqKey="Gallagher T" first="Thomas M." last="Gallagher">Thomas M. Gallagher</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, Loyola University Medical Center</s1><s2>Maywood, Illinois</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Illinois</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Coronavirus</term><term>Infection</term><term>Mechanism of action</term><term>Murine hepatitis virus</term><term>Protein</term><term>Severe acute respiratory syndrome</term><term>Virology</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Coronavirus</term><term>Virus hépatite murine</term><term>Protéine</term><term>Infection</term><term>Mécanisme action</term><term>Virologie</term><term>Syndrome respiratoire aigu sévère</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-p 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><li>Iowa</li></region><settlement><li>Iowa City</li></settlement><orgName><li>Université de l'Iowa</li></orgName></list><tree><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><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></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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