Impaired entry of soluble receptor-resistant mutants of mouse hepatitis virus into cells expressing MHVR2 receptor.
Identifieur interne : 006472 ( Main/Exploration ); précédent : 006471; suivant : 006473Impaired entry of soluble receptor-resistant mutants of mouse hepatitis virus into cells expressing MHVR2 receptor.
Auteurs : S. Matsuyama [Japon] ; F. TaguchiSource :
- Virology [ 0042-6822 ] ; 2000.
Descripteurs français
- KwdFr :
- Animaux, Antigène carcinoembryonnaire, Antigènes CD, Cellules géantes (cytologie), Cellules géantes (métabolisme), Cellules géantes (virologie), Cricetinae, Fusion cellulaire, Glycoprotéine de spicule des coronavirus, Glycoprotéines (génétique), Glycoprotéines (métabolisme), Glycoprotéines membranaires (génétique), Glycoprotéines membranaires (métabolisme), Lignée cellulaire, Membrane cellulaire (métabolisme), Molécules d'adhérence cellulaire, Mutation (génétique), Méthode des plages virales, Protéines de l'enveloppe virale (génétique), Protéines de l'enveloppe virale (métabolisme), Récepteurs viraux (génétique), Récepteurs viraux (métabolisme), Solubilité, Transfection, Virus de l'hépatite murine (croissance et développement), Virus de l'hépatite murine (génétique), Virus de l'hépatite murine (métabolisme), Virus de l'hépatite murine (physiologie).
- MESH :
- croissance et développement : Virus de l'hépatite murine.
- cytologie : Cellules géantes.
- génétique : Glycoprotéines, Glycoprotéines membranaires, Mutation, Protéines de l'enveloppe virale, Récepteurs viraux, Virus de l'hépatite murine.
- métabolisme : Cellules géantes, Glycoprotéines, Glycoprotéines membranaires, Membrane cellulaire, Protéines de l'enveloppe virale, Récepteurs viraux, Virus de l'hépatite murine.
- physiologie : Virus de l'hépatite murine.
- virologie : Cellules géantes.
- Animaux, Antigène carcinoembryonnaire, Antigènes CD, Cricetinae, Fusion cellulaire, Glycoprotéine de spicule des coronavirus, Lignée cellulaire, Molécules d'adhérence cellulaire, Méthode des plages virales, Solubilité, Transfection.
English descriptors
- KwdEn :
- Animals, Antigens, CD, Carcinoembryonic Antigen, Cell Adhesion Molecules, Cell Fusion, Cell Line, Cell Membrane (metabolism), Cricetinae, Giant Cells (cytology), Giant Cells (metabolism), Giant Cells (virology), Glycoproteins (genetics), Glycoproteins (metabolism), Membrane Glycoproteins (genetics), Membrane Glycoproteins (metabolism), Murine hepatitis virus (genetics), Murine hepatitis virus (growth & development), Murine hepatitis virus (metabolism), Murine hepatitis virus (physiology), Mutation (genetics), Receptors, Virus (genetics), Receptors, Virus (metabolism), Solubility, Spike Glycoprotein, Coronavirus, Transfection, Viral Envelope Proteins (genetics), Viral Envelope Proteins (metabolism), Viral Plaque Assay.
- MESH :
- chemical , genetics : Glycoproteins, Membrane Glycoproteins, Receptors, Virus, Viral Envelope Proteins.
- chemical , metabolism : Glycoproteins, Membrane Glycoproteins, Receptors, Virus, Viral Envelope Proteins.
- chemical : Antigens, CD, Carcinoembryonic Antigen, Cell Adhesion Molecules, Spike Glycoprotein, Coronavirus.
- cytology : Giant Cells.
- genetics : Murine hepatitis virus, Mutation.
- growth & development : Murine hepatitis virus.
- metabolism : Cell Membrane, Giant Cells, Murine hepatitis virus.
- physiology : Murine hepatitis virus.
- virology : Giant Cells.
- Animals, Cell Fusion, Cell Line, Cricetinae, Solubility, Transfection, Viral Plaque Assay.
Abstract
Mouse hepatitis virus (MHV) JHMV and its soluble receptor-resistant (srr) mutants, srr7, srr11, and srr18, grew and induced syncytia equally well in BHK-R1 cells expressing the MHVR1 receptor derived from MHV-susceptible BALB/c mice. In contrast, srr growth and syncytia formations were drastically reduced relative to wild-type (wt) virus in BHK-R2 cells expressing the MHVR2 receptor from MHV-resistant SJL mice. Infections by these srr mutants in BHK-R2 cells were 0.7 to 1.5 log10 less efficient than those of wt virus. BHK cells expressing both MHVR1 and MHVR2 supported srr replication to the same extent as did BHK-R1 cells, suggesting that inefficient infection by srr mutants in BHK-R2 cells resulted from the absence of the effective receptor MHVR1. Virus-receptor binding tests failed to demonstrate a difference between the abilities of wt and srr18 to bind MHVR2. The binding of srr7 and srr11 to both MHVR1 and MHVR2 was revealed lower by two- to fourfold relative to the wt binding. The fusion activity of srr S proteins as examined by the expression with recombinant vaccinia virus was apparently lower than that of the wt S protein in BHK-R2 cells, while there was not such a remarkable difference in BHK-R1 cells. This suggests that the most likely reason for inefficient infection by mutants in BHK-R2 is impaired virus entry into cells. These observations suggest that inefficient infections in BHK-R2 cells by srr mutants occur in the absence of a functional receptor MHVR1, which plays an important role in srr entry into cells.
DOI: 10.1006/viro.2000.0409
PubMed: 10891410
Affiliations:
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Le document en format XML
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Matsuyama</name><affiliation wicri:level="1"><nlm:affiliation>National Institute of Neuroscience, NCNP 4-1-1 Ogawahigashi, Kodaira, Tokyo, 187-8502, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>National Institute of Neuroscience, NCNP 4-1-1 Ogawahigashi, Kodaira, Tokyo, 187-8502</wicri:regionArea><wicri:noRegion>187-8502</wicri:noRegion></affiliation></author><author><name sortKey="Taguchi, F" sort="Taguchi, F" uniqKey="Taguchi F" first="F" last="Taguchi">F. Taguchi</name></author></analytic><series><title level="j">Virology</title><idno type="ISSN">0042-6822</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antigens, CD</term><term>Carcinoembryonic Antigen</term><term>Cell Adhesion Molecules</term><term>Cell Fusion</term><term>Cell Line</term><term>Cell Membrane (metabolism)</term><term>Cricetinae</term><term>Giant Cells (cytology)</term><term>Giant Cells (metabolism)</term><term>Giant Cells (virology)</term><term>Glycoproteins (genetics)</term><term>Glycoproteins (metabolism)</term><term>Membrane Glycoproteins (genetics)</term><term>Membrane Glycoproteins (metabolism)</term><term>Murine hepatitis virus (genetics)</term><term>Murine hepatitis virus (growth & development)</term><term>Murine hepatitis virus (metabolism)</term><term>Murine hepatitis virus (physiology)</term><term>Mutation (genetics)</term><term>Receptors, Virus (genetics)</term><term>Receptors, Virus (metabolism)</term><term>Solubility</term><term>Spike Glycoprotein, Coronavirus</term><term>Transfection</term><term>Viral Envelope Proteins (genetics)</term><term>Viral Envelope Proteins (metabolism)</term><term>Viral Plaque Assay</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antigène carcinoembryonnaire</term><term>Antigènes CD</term><term>Cellules géantes (cytologie)</term><term>Cellules géantes (métabolisme)</term><term>Cellules géantes (virologie)</term><term>Cricetinae</term><term>Fusion cellulaire</term><term>Glycoprotéine de spicule des coronavirus</term><term>Glycoprotéines (génétique)</term><term>Glycoprotéines (métabolisme)</term><term>Glycoprotéines membranaires (génétique)</term><term>Glycoprotéines membranaires (métabolisme)</term><term>Lignée cellulaire</term><term>Membrane cellulaire (métabolisme)</term><term>Molécules d'adhérence cellulaire</term><term>Mutation (génétique)</term><term>Méthode des plages virales</term><term>Protéines de l'enveloppe virale (génétique)</term><term>Protéines de l'enveloppe virale (métabolisme)</term><term>Récepteurs viraux (génétique)</term><term>Récepteurs viraux (métabolisme)</term><term>Solubilité</term><term>Transfection</term><term>Virus de l'hépatite murine (croissance et développement)</term><term>Virus de l'hépatite murine (génétique)</term><term>Virus de l'hépatite murine (métabolisme)</term><term>Virus de l'hépatite murine (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glycoproteins</term><term>Membrane Glycoproteins</term><term>Receptors, Virus</term><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glycoproteins</term><term>Membrane Glycoproteins</term><term>Receptors, Virus</term><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Antigens, CD</term><term>Carcinoembryonic Antigen</term><term>Cell Adhesion Molecules</term><term>Spike Glycoprotein, Coronavirus</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Virus de l'hépatite murine</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules géantes</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Giant Cells</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Murine hepatitis virus</term><term>Mutation</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>Glycoprotéines</term><term>Glycoprotéines membranaires</term><term>Mutation</term><term>Protéines de l'enveloppe 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xml:lang="en"><term>Animals</term><term>Cell Fusion</term><term>Cell Line</term><term>Cricetinae</term><term>Solubility</term><term>Transfection</term><term>Viral Plaque Assay</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Antigène carcinoembryonnaire</term><term>Antigènes CD</term><term>Cricetinae</term><term>Fusion cellulaire</term><term>Glycoprotéine de spicule des coronavirus</term><term>Lignée cellulaire</term><term>Molécules d'adhérence cellulaire</term><term>Méthode des plages virales</term><term>Solubilité</term><term>Transfection</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mouse hepatitis virus (MHV) JHMV and its soluble receptor-resistant (srr) mutants, srr7, srr11, and srr18, grew and induced syncytia equally well in BHK-R1 cells expressing the MHVR1 receptor derived from MHV-susceptible BALB/c mice. In contrast, srr growth and syncytia formations were drastically reduced relative to wild-type (wt) virus in BHK-R2 cells expressing the MHVR2 receptor from MHV-resistant SJL mice. Infections by these srr mutants in BHK-R2 cells were 0.7 to 1.5 log10 less efficient than those of wt virus. BHK cells expressing both MHVR1 and MHVR2 supported srr replication to the same extent as did BHK-R1 cells, suggesting that inefficient infection by srr mutants in BHK-R2 cells resulted from the absence of the effective receptor MHVR1. Virus-receptor binding tests failed to demonstrate a difference between the abilities of wt and srr18 to bind MHVR2. The binding of srr7 and srr11 to both MHVR1 and MHVR2 was revealed lower by two- to fourfold relative to the wt binding. The fusion activity of srr S proteins as examined by the expression with recombinant vaccinia virus was apparently lower than that of the wt S protein in BHK-R2 cells, while there was not such a remarkable difference in BHK-R1 cells. This suggests that the most likely reason for inefficient infection by mutants in BHK-R2 is impaired virus entry into cells. These observations suggest that inefficient infections in BHK-R2 cells by srr mutants occur in the absence of a functional receptor MHVR1, which plays an important role in srr entry into cells.</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><noCountry><name sortKey="Taguchi, F" sort="Taguchi, F" uniqKey="Taguchi F" first="F" last="Taguchi">F. Taguchi</name></noCountry><country name="Japon"><noRegion><name sortKey="Matsuyama, S" sort="Matsuyama, S" uniqKey="Matsuyama S" first="S" last="Matsuyama">S. Matsuyama</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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