The nsp1, nsp13, and M proteins contribute to the hepatotropism of murine coronavirus JHM.WU.
Identifieur interne : 001540 ( Main/Exploration ); précédent : 001539; suivant : 001541The nsp1, nsp13, and M proteins contribute to the hepatotropism of murine coronavirus JHM.WU.
Auteurs : Rong Zhang [États-Unis] ; Yize Li [États-Unis] ; Timothy J. Cowley [États-Unis] ; Adam D. Steinbrenner [États-Unis] ; Judith M. Phillips [États-Unis] ; Boyd L. Yount [États-Unis] ; Ralph S. Baric [États-Unis] ; Susan R. Weiss [États-Unis]Source :
- Journal of virology [ 1098-5514 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux, Cricetinae, Foie (virologie), Génétique inverse, Hépatite virale animale (virologie), Lignée cellulaire, Protéines de la matrice virale (génétique), Protéines de la matrice virale (métabolisme), Protéines virales non structurales (génétique), Protéines virales non structurales (métabolisme), Réplication virale, Souris de lignée C57BL, Tropisme viral, Virus de l'hépatite murine (génétique), Virus de l'hépatite murine (physiologie).
- MESH :
- génétique : Protéines de la matrice virale, Protéines virales non structurales, Virus de l'hépatite murine.
- métabolisme : Protéines de la matrice virale, Protéines virales non structurales.
- physiologie : Virus de l'hépatite murine.
- virologie : Foie, Hépatite virale animale.
- Animaux, Cricetinae, Génétique inverse, Lignée cellulaire, Réplication virale, Souris de lignée C57BL, Tropisme viral.
English descriptors
- KwdEn :
- Animals, Cell Line, Cricetinae, Hepatitis, Viral, Animal (virology), Liver (virology), Mice, Inbred C57BL, Murine hepatitis virus (genetics), Murine hepatitis virus (physiology), Reverse Genetics, Viral Matrix Proteins (genetics), Viral Matrix Proteins (metabolism), Viral Nonstructural Proteins (genetics), Viral Nonstructural Proteins (metabolism), Viral Tropism, Virus Replication.
- MESH :
- chemical , genetics : Viral Matrix Proteins, Viral Nonstructural Proteins.
- genetics : Murine hepatitis virus.
- chemical , metabolism : Viral Matrix Proteins, Viral Nonstructural Proteins.
- physiology : Murine hepatitis virus.
- virology : Hepatitis, Viral, Animal, Liver.
- Animals, Cell Line, Cricetinae, Mice, Inbred C57BL, Reverse Genetics, Viral Tropism, Virus Replication.
Abstract
Mouse hepatitis virus (MHV) isolates JHM.WU and JHM.SD promote severe central nervous system disease. However, while JHM.WU replicates robustly and induces hepatitis, JHM.SD fails to replicate or induce pathology in the liver. These two JHM variants encode homologous proteins with few polymorphisms, and little is known about which viral proteins(s) is responsible for the liver tropism of JHM.WU. We constructed reverse genetic systems for JHM.SD and JHM.WU and, utilizing these full-length cDNA clones, constructed chimeric viruses and mapped the virulence factors involved in liver tropism. Exchanging the spike proteins of the two viruses neither increased replication of JHM.SD in the liver nor attenuated JHM.WU. By further mapping, we found that polymorphisms in JHM.WU structural protein M and nonstructural replicase proteins nsp1 and nsp13 are essential for liver pathogenesis. M protein and nsp13, the helicase, of JHM.WU are required for efficient replication in vitro and in the liver in vivo. The JHM.SD nsp1 protein contains a K194R substitution of Lys194, a residue conserved among all other MHV strains. The K194R polymorphism has no effect on in vitro replication but influences hepatotropism, and introduction of R194K into JHM.SD promotes replication in the liver. Conversely, a K194R substitution in nsp1 of JHM.WU or A59, another hepatotropic strain, significantly attenuates replication of each strain in the liver and increases IFN-β expression in macrophages in culture. Our data indicate that both structural and nonstructural proteins contribute to MHV liver pathogenesis and support previous reports that nsp1 is a Betacoronavirus virulence factor.
DOI: 10.1128/JVI.03535-14
PubMed: 25589656
Affiliations:
- États-Unis
- Caroline du Nord, Pennsylvanie
- Chapel Hill (Caroline du Nord)
- Université de Caroline du Nord à Chapel Hill
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Le document en format XML
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Baric</name><affiliation wicri:level="4"><nlm:affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina</wicri:regionArea><placeName><region type="state">Caroline du Nord</region><settlement type="city">Chapel Hill (Caroline du Nord)</settlement></placeName><orgName type="university">Université de Caroline du Nord à Chapel Hill</orgName></affiliation></author><author><name sortKey="Weiss, Susan R" sort="Weiss, Susan R" uniqKey="Weiss S" first="Susan R" last="Weiss">Susan R. Weiss</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA weisssr@upenn.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania</wicri:regionArea><placeName><region type="state">Pennsylvanie</region></placeName></affiliation></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Cricetinae</term><term>Hepatitis, Viral, Animal (virology)</term><term>Liver (virology)</term><term>Mice, Inbred C57BL</term><term>Murine hepatitis virus (genetics)</term><term>Murine hepatitis virus (physiology)</term><term>Reverse Genetics</term><term>Viral Matrix Proteins (genetics)</term><term>Viral Matrix Proteins (metabolism)</term><term>Viral Nonstructural Proteins (genetics)</term><term>Viral Nonstructural Proteins (metabolism)</term><term>Viral Tropism</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cricetinae</term><term>Foie (virologie)</term><term>Génétique inverse</term><term>Hépatite virale animale (virologie)</term><term>Lignée cellulaire</term><term>Protéines de la matrice virale (génétique)</term><term>Protéines de la matrice virale (métabolisme)</term><term>Protéines virales non structurales (génétique)</term><term>Protéines virales non structurales (métabolisme)</term><term>Réplication virale</term><term>Souris de lignée C57BL</term><term>Tropisme viral</term><term>Virus de l'hépatite murine (génétique)</term><term>Virus de l'hépatite murine (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Viral Matrix Proteins</term><term>Viral Nonstructural Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Murine hepatitis virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines de la matrice virale</term><term>Protéines virales non structurales</term><term>Virus de l'hépatite murine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Viral Matrix Proteins</term><term>Viral Nonstructural Proteins</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines de la matrice virale</term><term>Protéines virales non structurales</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus de l'hépatite murine</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Murine hepatitis virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Foie</term><term>Hépatite virale animale</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Hepatitis, Viral, Animal</term><term>Liver</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Cricetinae</term><term>Mice, Inbred C57BL</term><term>Reverse Genetics</term><term>Viral Tropism</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cricetinae</term><term>Génétique inverse</term><term>Lignée cellulaire</term><term>Réplication virale</term><term>Souris de lignée C57BL</term><term>Tropisme viral</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mouse hepatitis virus (MHV) isolates JHM.WU and JHM.SD promote severe central nervous system disease. However, while JHM.WU replicates robustly and induces hepatitis, JHM.SD fails to replicate or induce pathology in the liver. These two JHM variants encode homologous proteins with few polymorphisms, and little is known about which viral proteins(s) is responsible for the liver tropism of JHM.WU. We constructed reverse genetic systems for JHM.SD and JHM.WU and, utilizing these full-length cDNA clones, constructed chimeric viruses and mapped the virulence factors involved in liver tropism. Exchanging the spike proteins of the two viruses neither increased replication of JHM.SD in the liver nor attenuated JHM.WU. By further mapping, we found that polymorphisms in JHM.WU structural protein M and nonstructural replicase proteins nsp1 and nsp13 are essential for liver pathogenesis. M protein and nsp13, the helicase, of JHM.WU are required for efficient replication in vitro and in the liver in vivo. The JHM.SD nsp1 protein contains a K194R substitution of Lys194, a residue conserved among all other MHV strains. The K194R polymorphism has no effect on in vitro replication but influences hepatotropism, and introduction of R194K into JHM.SD promotes replication in the liver. Conversely, a K194R substitution in nsp1 of JHM.WU or A59, another hepatotropic strain, significantly attenuates replication of each strain in the liver and increases IFN-β expression in macrophages in culture. Our data indicate that both structural and nonstructural proteins contribute to MHV liver pathogenesis and support previous reports that nsp1 is a Betacoronavirus virulence factor.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Caroline du Nord</li><li>Pennsylvanie</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="Pennsylvanie"><name sortKey="Zhang, Rong" sort="Zhang, Rong" uniqKey="Zhang R" first="Rong" last="Zhang">Rong Zhang</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="Cowley, Timothy J" sort="Cowley, Timothy J" uniqKey="Cowley T" first="Timothy J" last="Cowley">Timothy J. Cowley</name><name sortKey="Li, Yize" sort="Li, Yize" uniqKey="Li Y" first="Yize" last="Li">Yize Li</name><name sortKey="Phillips, Judith M" sort="Phillips, Judith M" uniqKey="Phillips J" first="Judith M" last="Phillips">Judith M. Phillips</name><name sortKey="Steinbrenner, Adam D" sort="Steinbrenner, Adam D" uniqKey="Steinbrenner A" first="Adam D" last="Steinbrenner">Adam D. Steinbrenner</name><name sortKey="Weiss, Susan R" sort="Weiss, Susan R" uniqKey="Weiss S" first="Susan R" last="Weiss">Susan R. Weiss</name><name sortKey="Yount, Boyd L" sort="Yount, Boyd L" uniqKey="Yount B" first="Boyd L" last="Yount">Boyd L. Yount</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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