Mouse Hepatitis Virus Strain JHM Infects a Human Hepatocellular Carcinoma Cell Line
Identifieur interne : 000694 ( Istex/Corpus ); précédent : 000693; suivant : 000695Mouse Hepatitis Virus Strain JHM Infects a Human Hepatocellular Carcinoma Cell Line
Auteurs : Peter J. Koetters ; Loubna Hassanieh ; Stephen A. Stohlman ; Thomas Gallagher ; Michael M. C. LaiSource :
- Virology [ 0042-6822 ] ; 1999.
English descriptors
- Teeft :
- Adoptive transfer, Assay, Baric, Biliary glycoprotein, Biol, Block infection, Cabirac, Carcinoma, Cause fusion, Cell fusion, Cell lines, Cell types, Chen, Coronavirus, Coronaviruses, Cultured cells, Demyelinating disease, Demyelination, Different animal species, Double staining, First hour, Fusion activity, Genomic structures, Glycoprotein, Growth curves, Hcea, Hensley, Hepatitis, Hepatocellular, Hepatotropic strain, Hepg2, Hepg2 cells, Host range, Howard hughes, Human cell line, Human cell lines, Human cells, Human coronavirus, Human disease, Human hepatocellular carcinoma cell line, Infection, Infects, Initial virus infection, Interspecies transfer, Lower virus titer, Mbgp, Monoclonal, Monoclonal antibodies, Monoclonal antibody, Mouse, Mouse cells, Mouse hepatitis virus, Mouse hepatitis virus entry, Mouse hepatitis virus receptors, Multiple sclerosis, Multiple sclerosis patients, Murine, Murine coronavirus spike protein, Murine coronaviruses, Neurotropic strain, Neutralizing antibody, Newborn calf serum, Other strains, Parental strains, Plaque, Plaque assay, Plaque formation, Plaque size, Postinfection, Primate, Protein expression, Protein production, Protein staining, Rabbit polyclonal antibody, Receptor, Receptor mbgp, Receptor specificity, Receptor utilization, Recombinant, Recombinant strains, Recombinant viruses, Replication, Room temperature, Same extent, Same mechanism, Sclerosis, Soluble form, Spike protein, Stohlman, Structural proteins, Syncytia formation, Syncytium, Titer, Transfected, Tryptone phosphate broth, Viral, Virol, Virology, Virus, Virus production, Virus replication, Virus strains, Virus titers, Yokomori.
Abstract
Abstract: Mouse hepatitis virus (MHV) strain JHM is a coronavirus that causes encephalitis and demyelination in susceptible rodents. The known receptors for MHV are all members of the carcinoembryonic antigen family. Although human forms of the MHV receptor can function as MHV receptors in some assays, no human cell line has been identified that can support wild-type MHV infection. Here we describe the infection of a human hepatocellular carcinoma cell line, HuH-7, with MHV. HuH-7 cells were susceptible to strains JHM-DL and JHM-DS, yielding virus titers nearly identical to those seen in mouse DBT cells. In contrast, HuH-7 cells were only marginally susceptible or completely resistant to infection by other MHV strains, including A59. JHM produced a strong cytopathic effect in HuH-7 cells with the formation of round plaques. Studies of various recombinant viruses between JHM and A59 strains suggested that the ability of JHM to infect HuH-7 cells was determined by multiple viral genetic elements. Blocking the viral spike (S) protein with a neutralizing antibody or a soluble form of the MHV receptor inhibited infection of HuH-7 cells, suggesting that infection is mediated through the S protein. Transfection with the prototype mouse receptor, biliary glycoprotein, rendered HuH-7 cells susceptible to infection by other MHV strains as well, suggesting that JHM uses a receptor distinct from the classical MHV receptor to infect HuH-7 cells. Possible implications for human disease are discussed.
Url:
DOI: 10.1006/viro.1999.9984
Links to Exploration step
ISTEX:1DFBB1E2397759A4EDFCCFF1C4527E2EFF21713ELe document en format XML
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Koetters</name><affiliation><mods:affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</mods:affiliation></affiliation></author><author><name sortKey="Hassanieh, Loubna" sort="Hassanieh, Loubna" uniqKey="Hassanieh L" first="Loubna" last="Hassanieh">Loubna Hassanieh</name><affiliation><mods:affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</mods:affiliation></affiliation></author><author><name sortKey="Stohlman, Stephen A" sort="Stohlman, Stephen A" uniqKey="Stohlman S" first="Stephen A." last="Stohlman">Stephen A. 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Koetters</name><affiliation><mods:affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</mods:affiliation></affiliation></author><author><name sortKey="Hassanieh, Loubna" sort="Hassanieh, Loubna" uniqKey="Hassanieh L" first="Loubna" last="Hassanieh">Loubna Hassanieh</name><affiliation><mods:affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</mods:affiliation></affiliation></author><author><name sortKey="Stohlman, Stephen A" sort="Stohlman, Stephen A" uniqKey="Stohlman S" first="Stephen A." last="Stohlman">Stephen A. 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Lai</name><affiliation><mods:affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="ISSN">0042-6822</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1999">1999</date><biblScope unit="volume">264</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="398">398</biblScope><biblScope unit="page" to="409">409</biblScope></imprint><idno type="ISSN">0042-6822</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0042-6822</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Adoptive transfer</term><term>Assay</term><term>Baric</term><term>Biliary glycoprotein</term><term>Biol</term><term>Block infection</term><term>Cabirac</term><term>Carcinoma</term><term>Cause fusion</term><term>Cell fusion</term><term>Cell lines</term><term>Cell types</term><term>Chen</term><term>Coronavirus</term><term>Coronaviruses</term><term>Cultured cells</term><term>Demyelinating disease</term><term>Demyelination</term><term>Different animal species</term><term>Double staining</term><term>First hour</term><term>Fusion activity</term><term>Genomic structures</term><term>Glycoprotein</term><term>Growth curves</term><term>Hcea</term><term>Hensley</term><term>Hepatitis</term><term>Hepatocellular</term><term>Hepatotropic strain</term><term>Hepg2</term><term>Hepg2 cells</term><term>Host range</term><term>Howard hughes</term><term>Human cell line</term><term>Human cell lines</term><term>Human cells</term><term>Human coronavirus</term><term>Human disease</term><term>Human hepatocellular carcinoma cell line</term><term>Infection</term><term>Infects</term><term>Initial virus infection</term><term>Interspecies transfer</term><term>Lower virus titer</term><term>Mbgp</term><term>Monoclonal</term><term>Monoclonal antibodies</term><term>Monoclonal antibody</term><term>Mouse</term><term>Mouse cells</term><term>Mouse hepatitis virus</term><term>Mouse hepatitis virus entry</term><term>Mouse hepatitis virus receptors</term><term>Multiple sclerosis</term><term>Multiple sclerosis patients</term><term>Murine</term><term>Murine coronavirus spike protein</term><term>Murine coronaviruses</term><term>Neurotropic strain</term><term>Neutralizing antibody</term><term>Newborn calf serum</term><term>Other strains</term><term>Parental strains</term><term>Plaque</term><term>Plaque assay</term><term>Plaque formation</term><term>Plaque size</term><term>Postinfection</term><term>Primate</term><term>Protein expression</term><term>Protein production</term><term>Protein staining</term><term>Rabbit polyclonal antibody</term><term>Receptor</term><term>Receptor mbgp</term><term>Receptor specificity</term><term>Receptor utilization</term><term>Recombinant</term><term>Recombinant strains</term><term>Recombinant viruses</term><term>Replication</term><term>Room temperature</term><term>Same extent</term><term>Same mechanism</term><term>Sclerosis</term><term>Soluble form</term><term>Spike protein</term><term>Stohlman</term><term>Structural proteins</term><term>Syncytia formation</term><term>Syncytium</term><term>Titer</term><term>Transfected</term><term>Tryptone phosphate broth</term><term>Viral</term><term>Virol</term><term>Virology</term><term>Virus</term><term>Virus production</term><term>Virus replication</term><term>Virus strains</term><term>Virus titers</term><term>Yokomori</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Mouse hepatitis virus (MHV) strain JHM is a coronavirus that causes encephalitis and demyelination in susceptible rodents. The known receptors for MHV are all members of the carcinoembryonic antigen family. Although human forms of the MHV receptor can function as MHV receptors in some assays, no human cell line has been identified that can support wild-type MHV infection. Here we describe the infection of a human hepatocellular carcinoma cell line, HuH-7, with MHV. HuH-7 cells were susceptible to strains JHM-DL and JHM-DS, yielding virus titers nearly identical to those seen in mouse DBT cells. In contrast, HuH-7 cells were only marginally susceptible or completely resistant to infection by other MHV strains, including A59. JHM produced a strong cytopathic effect in HuH-7 cells with the formation of round plaques. Studies of various recombinant viruses between JHM and A59 strains suggested that the ability of JHM to infect HuH-7 cells was determined by multiple viral genetic elements. Blocking the viral spike (S) protein with a neutralizing antibody or a soluble form of the MHV receptor inhibited infection of HuH-7 cells, suggesting that infection is mediated through the S protein. Transfection with the prototype mouse receptor, biliary glycoprotein, rendered HuH-7 cells susceptible to infection by other MHV strains as well, suggesting that JHM uses a receptor distinct from the classical MHV receptor to infect HuH-7 cells. 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Koetters</name><affiliations><json:string>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</json:string></affiliations></json:item><json:item><name>Loubna Hassanieh</name><affiliations><json:string>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</json:string></affiliations></json:item><json:item><name>Stephen A. Stohlman</name><affiliations><json:string>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</json:string></affiliations></json:item><json:item><name>Thomas Gallagher</name><affiliations><json:string>Loyola University Medical Center, Maywood, Illinois, 60153</json:string></affiliations></json:item><json:item><name>Michael M.C. Lai</name><affiliations><json:string>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</json:string></affiliations></json:item></author><arkIstex>ark:/67375/6H6-LXL2N7C8-V</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Mouse hepatitis virus (MHV) strain JHM is a coronavirus that causes encephalitis and demyelination in susceptible rodents. The known receptors for MHV are all members of the carcinoembryonic antigen family. Although human forms of the MHV receptor can function as MHV receptors in some assays, no human cell line has been identified that can support wild-type MHV infection. Here we describe the infection of a human hepatocellular carcinoma cell line, HuH-7, with MHV. HuH-7 cells were susceptible to strains JHM-DL and JHM-DS, yielding virus titers nearly identical to those seen in mouse DBT cells. In contrast, HuH-7 cells were only marginally susceptible or completely resistant to infection by other MHV strains, including A59. JHM produced a strong cytopathic effect in HuH-7 cells with the formation of round plaques. Studies of various recombinant viruses between JHM and A59 strains suggested that the ability of JHM to infect HuH-7 cells was determined by multiple viral genetic elements. Blocking the viral spike (S) protein with a neutralizing antibody or a soluble form of the MHV receptor inhibited infection of HuH-7 cells, suggesting that infection is mediated through the S protein. Transfection with the prototype mouse receptor, biliary glycoprotein, rendered HuH-7 cells susceptible to infection by other MHV strains as well, suggesting that JHM uses a receptor distinct from the classical MHV receptor to infect HuH-7 cells. Possible implications for human disease are discussed.</abstract><qualityIndicators><score>9.772</score><pdfWordCount>7065</pdfWordCount><pdfCharCount>41244</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>12</pdfPageCount><pdfPageSize>538 x 724 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>231</abstractWordCount><abstractCharCount>1511</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Mouse Hepatitis Virus Strain JHM Infects a Human Hepatocellular Carcinoma Cell Line</title><pmid><json:string>10562501</json:string></pmid><pii><json:string>S0042-6822(99)99984-1</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Virology</title><language><json:string>unknown</json:string></language><publicationDate>1999</publicationDate><issn><json:string>0042-6822</json:string></issn><pii><json:string>S0042-6822(00)X0058-X</json:string></pii><volume>264</volume><issue>2</issue><pages><first>398</first><last>409</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1999</json:string></date><geogName></geogName><orgName><json:string>Loyola University</json:string><json:string>Medical Center</json:string><json:string>American Qualex, San Clemente, CA</json:string><json:string>National Institutes of Health</json:string><json:string>Howard Hughes Medical Institute, University of Southern California Keck School of Medicine, Los Angeles, California</json:string><json:string>University of Southern California School of Medicine</json:string><json:string>American Type Culture Collection</json:string><json:string>Grant NS18146</json:string></orgName><orgName_funder><json:string>Grant NS18146</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Daphne Shimoda</json:string><json:string>Stephen A. Stohlman</json:string><json:string>Thomas Gallagher</json:string><json:string>Alan Epstein</json:string><json:string>Stephanie Shi</json:string><json:string>Loubna Hassanieh</json:string><json:string>M. C. Lai</json:string><json:string>Jerry Tuler</json:string></persName><placeName><json:string>Manassas</json:string><json:string>VA</json:string></placeName><ref_url><json:string>http://www.idealibrary.com</json:string></ref_url><ref_bibl><json:string>Yokomori et al., 1995</json:string><json:string>Lai and Stohlman, 1981</json:string><json:string>Yokomori and Lai, 1993</json:string><json:string>Gerdes et al., 1981</json:string><json:string>Hensley et al., 1998</json:string><json:string>Smith and Vanderplasschen, 1998</json:string><json:string>Stohlman et al., 1982</json:string><json:string>Goto et al., 1977</json:string><json:string>Yokomori and Lai, 1992, 1994</json:string><json:string>Schickli et al., 1997</json:string><json:string>Fleming et al., 1983, 1987</json:string><json:string>Wang et al., 1993</json:string><json:string>Makino et al., 1984</json:string><json:string>Yokomori and Lai, 1992</json:string><json:string>Chen et al., 1998</json:string><json:string>Dveksler et al., 1991</json:string><json:string>Powell and Lampert, 1975</json:string><json:string>Lai et al., 1981</json:string><json:string>Wang et al., 1992</json:string><json:string>Chen et al., 1995, 1997</json:string><json:string>Fleming et al., 1983</json:string><json:string>Nakabayashi et al., 1982</json:string><json:string>Gallagher, 1997</json:string><json:string>Weiss, 1983</json:string><json:string>Yokomori et al., 1993</json:string><json:string>Selinka et al., 1998</json:string><json:string>Compton et al., 1993</json:string><json:string>Hirano et al., 1974</json:string><json:string>Chen et al., 1997</json:string><json:string>Nagashima et al., 1978</json:string><json:string>Herndon et al., 1975</json:string><json:string>Kubo et al., 1994</json:string><json:string>Fleury et al., 1980</json:string><json:string>Cabirac et al., 1994</json:string><json:string>Zhang et al., 1998</json:string><json:string>Gallagher, 1996</json:string><json:string>Williams et al., 1990</json:string><json:string>Asanaka and Lai, 1993</json:string><json:string>Fleming et al., 1987</json:string><json:string>Kubo et al., 1993</json:string><json:string>Murray et al., 1992b, 1997</json:string><json:string>Geraghty et al., 1998</json:string><json:string>Lai, 1992</json:string><json:string>Burks et al., 1980</json:string><json:string>Yamamoto et al., 1990</json:string><json:string>Deregt et al., 1989</json:string><json:string>Chen et al., 1995</json:string><json:string>Hensley and Baric, 1998</json:string><json:string>Baric et al., 1999</json:string><json:string>Thoulouze et al., 1998</json:string><json:string>Watanabe et al., 1983</json:string><json:string>Dveksler et al., 1993</json:string><json:string>Hierholzer et al., 1979</json:string><json:string>Morris et al., 1989</json:string><json:string>Murray et al., 1992b</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-LXL2N7C8-V</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - virology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - virology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Virology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string><json:string>4 - tumeurs</json:string></inist></categories><publicationDate>1999</publicationDate><copyrightDate>1999</copyrightDate><doi><json:string>10.1006/viro.1999.9984</json:string></doi><id>1DFBB1E2397759A4EDFCCFF1C4527E2EFF21713E</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-LXL2N7C8-V/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-LXL2N7C8-V/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-LXL2N7C8-V/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Mouse Hepatitis Virus Strain JHM Infects a Human Hepatocellular Carcinoma Cell Line</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©1999 Academic Press</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>1999</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note type="content">Section title: Regular Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Mouse Hepatitis Virus Strain JHM Infects a Human Hepatocellular Carcinoma Cell Line</title><author xml:id="author-0000"><persName><forename type="first">Peter J.</forename><surname>Koetters</surname></persName><affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Loubna</forename><surname>Hassanieh</surname></persName><affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Stephen A.</forename><surname>Stohlman</surname></persName><affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Thomas</forename><surname>Gallagher</surname></persName><affiliation>Loyola University Medical Center, Maywood, Illinois, 60153</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Michael M.C.</forename><surname>Lai</surname></persName><note type="biography">To whom reprint requests should be addressed. Fax: (323) 342-9555. E-mail: michlai@hsc.usc.edu.</note><affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</affiliation></author><idno type="istex">1DFBB1E2397759A4EDFCCFF1C4527E2EFF21713E</idno><idno type="ark">ark:/67375/6H6-LXL2N7C8-V</idno><idno type="DOI">10.1006/viro.1999.9984</idno><idno type="PII">S0042-6822(99)99984-1</idno></analytic><monogr><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="pISSN">0042-6822</idno><idno type="PII">S0042-6822(00)X0058-X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1999"></date><biblScope unit="volume">264</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="398">398</biblScope><biblScope unit="page" to="409">409</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1999</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Mouse hepatitis virus (MHV) strain JHM is a coronavirus that causes encephalitis and demyelination in susceptible rodents. The known receptors for MHV are all members of the carcinoembryonic antigen family. Although human forms of the MHV receptor can function as MHV receptors in some assays, no human cell line has been identified that can support wild-type MHV infection. Here we describe the infection of a human hepatocellular carcinoma cell line, HuH-7, with MHV. HuH-7 cells were susceptible to strains JHM-DL and JHM-DS, yielding virus titers nearly identical to those seen in mouse DBT cells. In contrast, HuH-7 cells were only marginally susceptible or completely resistant to infection by other MHV strains, including A59. JHM produced a strong cytopathic effect in HuH-7 cells with the formation of round plaques. Studies of various recombinant viruses between JHM and A59 strains suggested that the ability of JHM to infect HuH-7 cells was determined by multiple viral genetic elements. Blocking the viral spike (S) protein with a neutralizing antibody or a soluble form of the MHV receptor inhibited infection of HuH-7 cells, suggesting that infection is mediated through the S protein. Transfection with the prototype mouse receptor, biliary glycoprotein, rendered HuH-7 cells susceptible to infection by other MHV strains as well, suggesting that JHM uses a receptor distinct from the classical MHV receptor to infect HuH-7 cells. Possible implications for human disease are discussed.</p></abstract></profileDesc><revisionDesc><change when="1999-07-06">Modified</change><change when="1999">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-LXL2N7C8-V/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>YVIRO</jid><aid>99984</aid><ce:pii>S0042-6822(99)99984-1</ce:pii><ce:doi>10.1006/viro.1999.9984</ce:doi><ce:copyright type="full-transfer" year="1999">Academic Press</ce:copyright></item-info><head><ce:dochead><ce:textfn>Regular Article</ce:textfn></ce:dochead><ce:title>Mouse Hepatitis Virus Strain JHM Infects a Human Hepatocellular Carcinoma Cell Line</ce:title><ce:author-group><ce:author><ce:given-name>Peter J.</ce:given-name><ce:surname>Koetters</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Loubna</ce:given-name><ce:surname>Hassanieh</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Stephen A.</ce:given-name><ce:surname>Stohlman</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Thomas</ce:given-name><ce:surname>Gallagher</ce:surname><ce:cross-ref refid="A3"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Michael M.C.</ce:given-name><ce:surname>Lai</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="A2"><ce:sup>c</ce:sup></ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="A1"><ce:label>a</ce:label><ce:textfn>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</ce:textfn></ce:affiliation><ce:affiliation id="A2"><ce:label>c</ce:label><ce:textfn>Howard Hughes Medical Institute, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</ce:textfn></ce:affiliation><ce:affiliation id="A3"><ce:label>b</ce:label><ce:textfn>Loyola University Medical Center, Maywood, Illinois, 60153</ce:textfn></ce:affiliation><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>To whom reprint requests should be addressed. Fax: (323) 342-9555. E-mail: michlai@hsc.usc.edu.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="26" month="5" year="1999"></ce:date-received><ce:date-revised day="6" month="7" year="1999"></ce:date-revised><ce:date-accepted day="25" month="8" year="1999"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Mouse hepatitis virus (MHV) strain JHM is a coronavirus that causes encephalitis and demyelination in susceptible rodents. The known receptors for MHV are all members of the carcinoembryonic antigen family. Although human forms of the MHV receptor can function as MHV receptors in some assays, no human cell line has been identified that can support wild-type MHV infection. Here we describe the infection of a human hepatocellular carcinoma cell line, HuH-7, with MHV. HuH-7 cells were susceptible to strains JHM-DL and JHM-DS, yielding virus titers nearly identical to those seen in mouse DBT cells. In contrast, HuH-7 cells were only marginally susceptible or completely resistant to infection by other MHV strains, including A59. JHM produced a strong cytopathic effect in HuH-7 cells with the formation of round plaques. Studies of various recombinant viruses between JHM and A59 strains suggested that the ability of JHM to infect HuH-7 cells was determined by multiple viral genetic elements. Blocking the viral spike (S) protein with a neutralizing antibody or a soluble form of the MHV receptor inhibited infection of HuH-7 cells, suggesting that infection is mediated through the S protein. Transfection with the prototype mouse receptor, biliary glycoprotein, rendered HuH-7 cells susceptible to infection by other MHV strains as well, suggesting that JHM uses a receptor distinct from the classical MHV receptor to infect HuH-7 cells. Possible implications for human disease are discussed.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Mouse Hepatitis Virus Strain JHM Infects a Human Hepatocellular Carcinoma Cell Line</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Mouse Hepatitis Virus Strain JHM Infects a Human Hepatocellular Carcinoma Cell Line</title></titleInfo><name type="personal"><namePart type="given">Peter J.</namePart><namePart type="family">Koetters</namePart><affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Loubna</namePart><namePart type="family">Hassanieh</namePart><affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stephen A.</namePart><namePart type="family">Stohlman</namePart><affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Gallagher</namePart><affiliation>Loyola University Medical Center, Maywood, Illinois, 60153</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael M.C.</namePart><namePart type="family">Lai</namePart><affiliation>Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, 90033</affiliation><description>To whom reprint requests should be addressed. Fax: (323) 342-9555. E-mail: michlai@hsc.usc.edu.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1999</dateIssued><dateModified encoding="w3cdtf">1999-07-06</dateModified><copyrightDate encoding="w3cdtf">1999</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Mouse hepatitis virus (MHV) strain JHM is a coronavirus that causes encephalitis and demyelination in susceptible rodents. The known receptors for MHV are all members of the carcinoembryonic antigen family. Although human forms of the MHV receptor can function as MHV receptors in some assays, no human cell line has been identified that can support wild-type MHV infection. Here we describe the infection of a human hepatocellular carcinoma cell line, HuH-7, with MHV. HuH-7 cells were susceptible to strains JHM-DL and JHM-DS, yielding virus titers nearly identical to those seen in mouse DBT cells. In contrast, HuH-7 cells were only marginally susceptible or completely resistant to infection by other MHV strains, including A59. JHM produced a strong cytopathic effect in HuH-7 cells with the formation of round plaques. Studies of various recombinant viruses between JHM and A59 strains suggested that the ability of JHM to infect HuH-7 cells was determined by multiple viral genetic elements. Blocking the viral spike (S) protein with a neutralizing antibody or a soluble form of the MHV receptor inhibited infection of HuH-7 cells, suggesting that infection is mediated through the S protein. Transfection with the prototype mouse receptor, biliary glycoprotein, rendered HuH-7 cells susceptible to infection by other MHV strains as well, suggesting that JHM uses a receptor distinct from the classical MHV receptor to infect HuH-7 cells. Possible implications for human disease are discussed.</abstract><note type="content">Section title: Regular Article</note><relatedItem type="host"><titleInfo><title>Virology</title></titleInfo><titleInfo type="abbreviated"><title>YVIRO</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1999</dateIssued></originInfo><identifier type="ISSN">0042-6822</identifier><identifier type="PII">S0042-6822(00)X0058-X</identifier><part><date>1999</date><detail type="volume"><number>264</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>245</start><end>453</end></extent><extent unit="pages"><start>398</start><end>409</end></extent></part></relatedItem><identifier type="istex">1DFBB1E2397759A4EDFCCFF1C4527E2EFF21713E</identifier><identifier type="ark">ark:/67375/6H6-LXL2N7C8-V</identifier><identifier type="DOI">10.1006/viro.1999.9984</identifier><identifier type="PII">S0042-6822(99)99984-1</identifier><accessCondition type="use and reproduction" contentType="copyright">©1999 Academic Press</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Academic Press, ©1999</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-LXL2N7C8-V/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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