In vivo and in vitro models of demyelinating disease. XVII. The infectious process in athymic rats inoculated with JHM virus
Identifieur interne : 000152 ( Istex/Corpus ); précédent : 000151; suivant : 000153In vivo and in vitro models of demyelinating disease. XVII. The infectious process in athymic rats inoculated with JHM virus
Auteurs : O. Sorensen ; A. Saravani ; S. DalesSource :
- Microbial Pathogenesis [ 0882-4010 ] ; 1987.
English descriptors
- Teeft :
- Acta neuropathol, Asymptomatic, Athymic, Athymic rats, Athymic rats inoculated, Cdna probes, Cell functions, Cellular, Cellular immunity, Cerebellum, Clin lmmunol lmmunopathol, Clinical symptoms, Demyelinating, Demyelinating disease, Demyelinating diseases, Disease process, Disease symptoms, Euthymic, Euthymic animals, Euthymic rats, Extensive destruction, Extensive infiltration, Heterozygous, Hind limbs, Hippocampal neurons, Hybridization, Infectious process, Infiltrates, Inoculated, Inoculation, Jhmv, Jhmv infection, Latency period, Lateral ventricle, Lesion, Microbial pathogenesis, Mononuclear, Mononuclear cells, Myelencephalon, Natural cytotoxicity, Neuron, Nude rats, Nude rats inoculated, Older rats, Paralysed, Present data, Primary explants, Rat, Rats inoculated, Sorensen, Spinal, Spinal cord, Target cells, Tissue damage, Tissue sections, Various ages, Virus infection, White matter, Wistar lewis.
Abstract
Abstract: Wistar Lewis (WL), Long Evans (LE) and other rat strains develop complete resistance to CNS disease when inoculated intracerebrally with murine hepatitis JHM virus (JHMV) after the 10th day of age.11Sorensen O, Percy D, Dales S. In vivo and in vitro models of demyelinating diseases. III. JHM virus infection of rats. Arch Neurol 1980; 37: 478-84. Two types of studies were conducted to ascertain the involvement of the cellular immune system in development of resistance. Immunosuppression of WL rats with cyclosporin A (CsA) following onset of the age-related resistance demonstrated that this drug was partially able to abrogate resistance. In the other studies nude (rnu/rnu) rats, their heterozygous (rnu/+) litter mates and genetically related LE rats of various ages were challenged with JHMV. The rnu/+ and LE animals became completely resistant before the age of weaning, whereas some rnu/rnu rats, challenged as late as 70 days of age, showed disease symptoms—albeit after a long latent period. These observations indicated that the cellular immune system plays an important role in suppressing the disease process in the CNS. When the infection of nude rats was initiated on or after the 15th day of life, the histological lesions were generally small and present in both grey and white matter but were seldom seen in the spinal cord. Mononuclear infiltrates were evident throughout the CNS. In some nude rats there was massive mononuclear cell infiltration towards the meningies and into ventricular spaces. By contrast in rnu/+, LE and WL rats with late-onset disease symptoms, demyelinating-type lesions were confined to the white matter and only minor infiltration of mononuclear cells was evident. JHMV RNA was detectable by dot-blotting analysis in the CNS of both paralysed and asymptomatic rnu/rnu and rnu/+ rats, but less RNA was usually detected in heterozygous animals. In-situ hybridization with cDNA probes for JHMV RNA showed that neurons in the hippocampus and cerebellum, as well as cells in the white matter, were frequently infected. The present data indicate that in the rat T cells have an important function in maintaining resistance to the JHMV related disease process. However, even without a functional T cell compartment nude rats challenged after 15 days of age did not develop an acute encephalitis, suggesting that an age-dependent, non-immunological mechanism is also involved in restricting the spread of infection. It is possible that resistance in euthymic rats sets in because: (1) at the time of weaning the CNS matures, so that the number of targets available for infection is reduced, (2) T cells prevent the late-onset disease by clearing persistent, low grade infections from the CNS.
Url:
DOI: 10.1016/0882-4010(87)90100-8
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Sorensen</name><affiliation><mods:affiliation>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</mods:affiliation></affiliation></author><author><name sortKey="Saravani, A" sort="Saravani, A" uniqKey="Saravani A" first="A." last="Saravani">A. Saravani</name><affiliation><mods:affiliation>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</mods:affiliation></affiliation></author><author><name sortKey="Dales, S" sort="Dales, S" uniqKey="Dales S" first="S." last="Dales">S. Dales</name><affiliation><mods:affiliation>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Microbial Pathogenesis</title><title level="j" type="abbrev">YMPAT</title><idno type="ISSN">0882-4010</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1987">1987</date><biblScope unit="volume">2</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="79">79</biblScope><biblScope unit="page" to="90">90</biblScope></imprint><idno type="ISSN">0882-4010</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0882-4010</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acta neuropathol</term><term>Asymptomatic</term><term>Athymic</term><term>Athymic rats</term><term>Athymic rats inoculated</term><term>Cdna probes</term><term>Cell functions</term><term>Cellular</term><term>Cellular immunity</term><term>Cerebellum</term><term>Clin lmmunol lmmunopathol</term><term>Clinical symptoms</term><term>Demyelinating</term><term>Demyelinating disease</term><term>Demyelinating diseases</term><term>Disease process</term><term>Disease symptoms</term><term>Euthymic</term><term>Euthymic animals</term><term>Euthymic rats</term><term>Extensive destruction</term><term>Extensive infiltration</term><term>Heterozygous</term><term>Hind limbs</term><term>Hippocampal neurons</term><term>Hybridization</term><term>Infectious process</term><term>Infiltrates</term><term>Inoculated</term><term>Inoculation</term><term>Jhmv</term><term>Jhmv infection</term><term>Latency period</term><term>Lateral ventricle</term><term>Lesion</term><term>Microbial pathogenesis</term><term>Mononuclear</term><term>Mononuclear cells</term><term>Myelencephalon</term><term>Natural cytotoxicity</term><term>Neuron</term><term>Nude rats</term><term>Nude rats inoculated</term><term>Older rats</term><term>Paralysed</term><term>Present data</term><term>Primary explants</term><term>Rat</term><term>Rats inoculated</term><term>Sorensen</term><term>Spinal</term><term>Spinal cord</term><term>Target cells</term><term>Tissue damage</term><term>Tissue sections</term><term>Various ages</term><term>Virus infection</term><term>White matter</term><term>Wistar lewis</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Wistar Lewis (WL), Long Evans (LE) and other rat strains develop complete resistance to CNS disease when inoculated intracerebrally with murine hepatitis JHM virus (JHMV) after the 10th day of age.11Sorensen O, Percy D, Dales S. In vivo and in vitro models of demyelinating diseases. III. JHM virus infection of rats. Arch Neurol 1980; 37: 478-84. Two types of studies were conducted to ascertain the involvement of the cellular immune system in development of resistance. Immunosuppression of WL rats with cyclosporin A (CsA) following onset of the age-related resistance demonstrated that this drug was partially able to abrogate resistance. In the other studies nude (rnu/rnu) rats, their heterozygous (rnu/+) litter mates and genetically related LE rats of various ages were challenged with JHMV. The rnu/+ and LE animals became completely resistant before the age of weaning, whereas some rnu/rnu rats, challenged as late as 70 days of age, showed disease symptoms—albeit after a long latent period. These observations indicated that the cellular immune system plays an important role in suppressing the disease process in the CNS. When the infection of nude rats was initiated on or after the 15th day of life, the histological lesions were generally small and present in both grey and white matter but were seldom seen in the spinal cord. Mononuclear infiltrates were evident throughout the CNS. In some nude rats there was massive mononuclear cell infiltration towards the meningies and into ventricular spaces. By contrast in rnu/+, LE and WL rats with late-onset disease symptoms, demyelinating-type lesions were confined to the white matter and only minor infiltration of mononuclear cells was evident. JHMV RNA was detectable by dot-blotting analysis in the CNS of both paralysed and asymptomatic rnu/rnu and rnu/+ rats, but less RNA was usually detected in heterozygous animals. In-situ hybridization with cDNA probes for JHMV RNA showed that neurons in the hippocampus and cerebellum, as well as cells in the white matter, were frequently infected. The present data indicate that in the rat T cells have an important function in maintaining resistance to the JHMV related disease process. However, even without a functional T cell compartment nude rats challenged after 15 days of age did not develop an acute encephalitis, suggesting that an age-dependent, non-immunological mechanism is also involved in restricting the spread of infection. It is possible that resistance in euthymic rats sets in because: (1) at the time of weaning the CNS matures, so that the number of targets available for infection is reduced, (2) T cells prevent the late-onset disease by clearing persistent, low grade infections from the CNS.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>jhmv</json:string><json:string>inoculated</json:string><json:string>demyelinating</json:string><json:string>athymic</json:string><json:string>nude rats</json:string><json:string>demyelinating disease</json:string><json:string>sorensen</json:string><json:string>myelencephalon</json:string><json:string>spinal cord</json:string><json:string>spinal</json:string><json:string>hybridization</json:string><json:string>mononuclear cells</json:string><json:string>white matter</json:string><json:string>euthymic</json:string><json:string>infiltrates</json:string><json:string>asymptomatic</json:string><json:string>paralysed</json:string><json:string>rat</json:string><json:string>cerebellum</json:string><json:string>mononuclear</json:string><json:string>neuron</json:string><json:string>cellular immunity</json:string><json:string>disease process</json:string><json:string>various ages</json:string><json:string>athymic rats</json:string><json:string>lesion</json:string><json:string>inoculation</json:string><json:string>disease symptoms</json:string><json:string>primary explants</json:string><json:string>cdna probes</json:string><json:string>cell functions</json:string><json:string>nude rats inoculated</json:string><json:string>infectious process</json:string><json:string>euthymic rats</json:string><json:string>virus infection</json:string><json:string>tissue sections</json:string><json:string>demyelinating diseases</json:string><json:string>cellular</json:string><json:string>clinical symptoms</json:string><json:string>microbial pathogenesis</json:string><json:string>jhmv infection</json:string><json:string>older rats</json:string><json:string>hind limbs</json:string><json:string>tissue damage</json:string><json:string>rats inoculated</json:string><json:string>latency period</json:string><json:string>athymic rats inoculated</json:string><json:string>clin lmmunol lmmunopathol</json:string><json:string>extensive destruction</json:string><json:string>hippocampal neurons</json:string><json:string>target cells</json:string><json:string>euthymic animals</json:string><json:string>extensive infiltration</json:string><json:string>lateral ventricle</json:string><json:string>wistar lewis</json:string><json:string>present data</json:string><json:string>acta neuropathol</json:string><json:string>natural cytotoxicity</json:string><json:string>heterozygous</json:string></teeft></keywords><author><json:item><name>O. Sorensen</name><affiliations><json:string>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</json:string></affiliations></json:item><json:item><name>A. Saravani</name><affiliations><json:string>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</json:string></affiliations></json:item><json:item><name>S. Dales</name><affiliations><json:string>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>nude rats</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>coronavirus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CNS disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>demyelination</value></json:item></subject><arkIstex>ark:/67375/6H6-LH37PTBP-9</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Wistar Lewis (WL), Long Evans (LE) and other rat strains develop complete resistance to CNS disease when inoculated intracerebrally with murine hepatitis JHM virus (JHMV) after the 10th day of age.11Sorensen O, Percy D, Dales S. In vivo and in vitro models of demyelinating diseases. III. JHM virus infection of rats. Arch Neurol 1980; 37: 478-84. Two types of studies were conducted to ascertain the involvement of the cellular immune system in development of resistance. Immunosuppression of WL rats with cyclosporin A (CsA) following onset of the age-related resistance demonstrated that this drug was partially able to abrogate resistance. In the other studies nude (rnu/rnu) rats, their heterozygous (rnu/+) litter mates and genetically related LE rats of various ages were challenged with JHMV. The rnu/+ and LE animals became completely resistant before the age of weaning, whereas some rnu/rnu rats, challenged as late as 70 days of age, showed disease symptoms—albeit after a long latent period. These observations indicated that the cellular immune system plays an important role in suppressing the disease process in the CNS. When the infection of nude rats was initiated on or after the 15th day of life, the histological lesions were generally small and present in both grey and white matter but were seldom seen in the spinal cord. Mononuclear infiltrates were evident throughout the CNS. In some nude rats there was massive mononuclear cell infiltration towards the meningies and into ventricular spaces. By contrast in rnu/+, LE and WL rats with late-onset disease symptoms, demyelinating-type lesions were confined to the white matter and only minor infiltration of mononuclear cells was evident. JHMV RNA was detectable by dot-blotting analysis in the CNS of both paralysed and asymptomatic rnu/rnu and rnu/+ rats, but less RNA was usually detected in heterozygous animals. In-situ hybridization with cDNA probes for JHMV RNA showed that neurons in the hippocampus and cerebellum, as well as cells in the white matter, were frequently infected. The present data indicate that in the rat T cells have an important function in maintaining resistance to the JHMV related disease process. However, even without a functional T cell compartment nude rats challenged after 15 days of age did not develop an acute encephalitis, suggesting that an age-dependent, non-immunological mechanism is also involved in restricting the spread of infection. It is possible that resistance in euthymic rats sets in because: (1) at the time of weaning the CNS matures, so that the number of targets available for infection is reduced, (2) T cells prevent the late-onset disease by clearing persistent, low grade infections from the CNS.</abstract><qualityIndicators><score>7.717</score><pdfWordCount>2717</pdfWordCount><pdfCharCount>25875</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>12</pdfPageCount><pdfPageSize>489.28 x 704.56 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>430</abstractWordCount><abstractCharCount>2743</abstractCharCount><keywordCount>4</keywordCount></qualityIndicators><title>In vivo and in vitro models of demyelinating disease. XVII. The infectious process in athymic rats inoculated with JHM virus</title><pmid><json:string>2853273</json:string></pmid><pii><json:string>0882-4010(87)90100-8</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Microbial Pathogenesis</title><language><json:string>unknown</json:string></language><publicationDate>1987</publicationDate><issn><json:string>0882-4010</json:string></issn><pii><json:string>S0882-4010(00)X0196-9</json:string></pii><volume>2</volume><issue>2</issue><pages><first>79</first><last>90</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>32S</json:string><json:string>1987</json:string><json:string>35S</json:string></date><geogName></geogName><orgName><json:string>Hospital Ltd</json:string><json:string>Canadian Breeding Laboratories</json:string><json:string>Department of Microbiology and Infectious Diseases</json:string><json:string>University of Western</json:string><json:string>A Canada Inc</json:string><json:string>University of Western Ontario</json:string><json:string>MS Society of Canada</json:string><json:string>MRC</json:string></orgName><orgName_funder><json:string>MS Society of Canada</json:string><json:string>MRC</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Harlan Sprague</json:string><json:string>L. Chow</json:string><json:string>A. Saravani</json:string><json:string>Charles River</json:string><json:string>Lesions</json:string><json:string>Long Evans</json:string><json:string>S. Dales</json:string></persName><placeName><json:string>Calgary</json:string><json:string>Montreal</json:string><json:string>St Contant</json:string><json:string>Canada</json:string><json:string>Quebec</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>University Academic of Calgary, 3330</json:string><json:string>Sorensen et al.</json:string><json:string>Vos et al.</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-LH37PTBP-9</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - microbiology</json:string><json:string>2 - immunology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - microbiology</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Infectious Diseases</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Microbiology</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></inist></categories><publicationDate>1987</publicationDate><copyrightDate>1987</copyrightDate><doi><json:string>10.1016/0882-4010(87)90100-8</json:string></doi><id>8AA99663F1B420905279642F839412D56765E817</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-LH37PTBP-9/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-LH37PTBP-9/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-LH37PTBP-9/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">In vivo and in vitro models of demyelinating disease. XVII. The infectious process in athymic rats inoculated with JHM virus</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>elsevier</p></licence></availability><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p><date>1987</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>Supported by grants from the MS Society of Canada and the MRC of Canada.</note><note type="content">Section title: Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">In vivo and in vitro models of demyelinating disease. XVII. The infectious process in athymic rats inoculated with JHM virus</title><author xml:id="author-0000"><persName><forename type="first">O.</forename><surname>Sorensen</surname></persName><note type="biography">Present adress: Department of Microbiology and Infectious Diseases, University of Calgary, 3330 Hospital Drive N.W., Calgary, Alberta, Canada T2N 4N1.</note><affiliation>Present adress: Department of Microbiology and Infectious Diseases, University of Calgary, 3330 Hospital Drive N.W., Calgary, Alberta, Canada T2N 4N1.</affiliation><affiliation>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</affiliation></author><author xml:id="author-0001"><persName><forename type="first">A.</forename><surname>Saravani</surname></persName><affiliation>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</affiliation></author><author xml:id="author-0002"><persName><forename type="first">S.</forename><surname>Dales</surname></persName><note type="biography">Author to whom reprint requests should be addressed.</note><affiliation>Author to whom reprint requests should be addressed.</affiliation><affiliation>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</affiliation></author><idno type="istex">8AA99663F1B420905279642F839412D56765E817</idno><idno type="ark">ark:/67375/6H6-LH37PTBP-9</idno><idno type="DOI">10.1016/0882-4010(87)90100-8</idno><idno type="PII">0882-4010(87)90100-8</idno></analytic><monogr><title level="j">Microbial Pathogenesis</title><title level="j" type="abbrev">YMPAT</title><idno type="pISSN">0882-4010</idno><idno type="PII">S0882-4010(00)X0196-9</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1987"></date><biblScope unit="volume">2</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="79">79</biblScope><biblScope unit="page" to="90">90</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1987</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Wistar Lewis (WL), Long Evans (LE) and other rat strains develop complete resistance to CNS disease when inoculated intracerebrally with murine hepatitis JHM virus (JHMV) after the 10th day of age.11Sorensen O, Percy D, Dales S. In vivo and in vitro models of demyelinating diseases. III. JHM virus infection of rats. Arch Neurol 1980; 37: 478-84. Two types of studies were conducted to ascertain the involvement of the cellular immune system in development of resistance. Immunosuppression of WL rats with cyclosporin A (CsA) following onset of the age-related resistance demonstrated that this drug was partially able to abrogate resistance. In the other studies nude (rnu/rnu) rats, their heterozygous (rnu/+) litter mates and genetically related LE rats of various ages were challenged with JHMV. The rnu/+ and LE animals became completely resistant before the age of weaning, whereas some rnu/rnu rats, challenged as late as 70 days of age, showed disease symptoms—albeit after a long latent period. These observations indicated that the cellular immune system plays an important role in suppressing the disease process in the CNS. When the infection of nude rats was initiated on or after the 15th day of life, the histological lesions were generally small and present in both grey and white matter but were seldom seen in the spinal cord. Mononuclear infiltrates were evident throughout the CNS. In some nude rats there was massive mononuclear cell infiltration towards the meningies and into ventricular spaces. By contrast in rnu/+, LE and WL rats with late-onset disease symptoms, demyelinating-type lesions were confined to the white matter and only minor infiltration of mononuclear cells was evident. JHMV RNA was detectable by dot-blotting analysis in the CNS of both paralysed and asymptomatic rnu/rnu and rnu/+ rats, but less RNA was usually detected in heterozygous animals. In-situ hybridization with cDNA probes for JHMV RNA showed that neurons in the hippocampus and cerebellum, as well as cells in the white matter, were frequently infected. The present data indicate that in the rat T cells have an important function in maintaining resistance to the JHMV related disease process. However, even without a functional T cell compartment nude rats challenged after 15 days of age did not develop an acute encephalitis, suggesting that an age-dependent, non-immunological mechanism is also involved in restricting the spread of infection. It is possible that resistance in euthymic rats sets in because: (1) at the time of weaning the CNS matures, so that the number of targets available for infection is reduced, (2) T cells prevent the late-onset disease by clearing persistent, low grade infections from the CNS.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>nude rats</term></item><item><term>coronavirus</term></item><item><term>CNS disease</term></item><item><term>demyelination</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1987">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-LH37PTBP-9/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"><item-info><jid>YMPAT</jid><aid>87901008</aid><ce:pii>0882-4010(87)90100-8</ce:pii><ce:doi>10.1016/0882-4010(87)90100-8</ce:doi><ce:copyright type="unknown" year="1987"></ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>Supported by grants from the MS Society of Canada and the MRC of Canada.</ce:note-para></ce:article-footnote><ce:dochead><ce:textfn>Article</ce:textfn></ce:dochead><ce:title><ce:italic>In vivo</ce:italic> and <ce:italic>in vitro</ce:italic> models of demyelinating disease. XVII. The infectious process in athymic rats inoculated with JHM virus</ce:title><ce:author-group><ce:author><ce:given-name>O.</ce:given-name><ce:surname>Sorensen</ce:surname><ce:cross-ref refid="FN2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>A.</ce:given-name><ce:surname>Saravani</ce:surname></ce:author><ce:author><ce:given-name>S.</ce:given-name><ce:surname>Dales</ce:surname><ce:cross-ref refid="COR1"><ce:sup>‡</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>‡</ce:label><ce:text>Author to whom reprint requests should be addressed.</ce:text></ce:correspondence><ce:footnote id="FN2"><ce:label>†</ce:label><ce:note-para>Present adress: Department of Microbiology and Infectious Diseases, University of Calgary, 3330 Hospital Drive N.W., Calgary, Alberta, Canada T2N 4N1.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="13" month="3" year="1986"></ce:date-received><ce:date-accepted day="25" month="8" year="1986"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Wistar Lewis (WL), Long Evans (LE) and other rat strains develop complete resistance to CNS disease when inoculated intracerebrally with murine hepatitis JHM virus (JHMV) after the 10th day of age.<ce:cross-ref refid="FN1"><ce:sup>1</ce:sup></ce:cross-ref><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>Sorensen O, Percy D, Dales S. <ce:italic>In vivo</ce:italic> and <ce:italic>in vitro</ce:italic> models of demyelinating diseases. III. JHM virus infection of rats. Arch Neurol 1980; 37: 478-84.</ce:note-para></ce:footnote> Two types of studies were conducted to ascertain the involvement of the cellular immune system in development of resistance. Immunosuppression of WL rats with cyclosporin A (CsA) following onset of the age-related resistance demonstrated that this drug was partially able to abrogate resistance. In the other studies nude (rnu/rnu) rats, their heterozygous (rnu/+) litter mates and genetically related LE rats of various ages were challenged with JHMV. The rnu/+ and LE animals became completely resistant before the age of weaning, whereas some rnu/rnu rats, challenged as late as 70 days of age, showed disease symptoms—albeit after a long latent period. These observations indicated that the cellular immune system plays an important role in suppressing the disease process in the CNS. When the infection of nude rats was initiated on or after the 15th day of life, the histological lesions were generally small and present in both grey and white matter but were seldom seen in the spinal cord. Mononuclear infiltrates were evident throughout the CNS. In some nude rats there was massive mononuclear cell infiltration towards the meningies and into ventricular spaces. By contrast in rnu/+, LE and WL rats with late-onset disease symptoms, demyelinating-type lesions were confined to the white matter and only minor infiltration of mononuclear cells was evident. JHMV RNA was detectable by dot-blotting analysis in the CNS of both paralysed and asymptomatic rnu/rnu and rnu/+ rats, but less RNA was usually detected in heterozygous animals. <ce:italic>In-situ</ce:italic> hybridization with cDNA probes for JHMV RNA showed that neurons in the hippocampus and cerebellum, as well as cells in the white matter, were frequently infected. The present data indicate that in the rat T cells have an important function in maintaining resistance to the JHMV related disease process. However, even without a functional T cell compartment nude rats challenged after 15 days of age did not develop an acute encephalitis, suggesting that an age-dependent, non-immunological mechanism is also involved in restricting the spread of infection. It is possible that resistance in euthymic rats sets in because: (1) at the time of weaning the CNS matures, so that the number of targets available for infection is reduced, (2) T cells prevent the late-onset disease by clearing persistent, low grade infections from the CNS.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>nude rats</ce:text></ce:keyword><ce:keyword><ce:text>coronavirus</ce:text></ce:keyword><ce:keyword><ce:text>CNS disease</ce:text></ce:keyword><ce:keyword><ce:text>demyelination</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>In vivo and in vitro models of demyelinating disease. XVII. The infectious process in athymic rats inoculated with JHM virus</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>and</title></titleInfo><name type="personal"><namePart type="given">O.</namePart><namePart type="family">Sorensen</namePart><affiliation>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</affiliation><description>Present adress: Department of Microbiology and Infectious Diseases, University of Calgary, 3330 Hospital Drive N.W., Calgary, Alberta, Canada T2N 4N1.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Saravani</namePart><affiliation>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Dales</namePart><affiliation>Cytobiology Group, Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada N6A 5C1</affiliation><description>Author to whom reprint requests should be addressed.</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">1987</dateIssued><copyrightDate encoding="w3cdtf">1987</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Wistar Lewis (WL), Long Evans (LE) and other rat strains develop complete resistance to CNS disease when inoculated intracerebrally with murine hepatitis JHM virus (JHMV) after the 10th day of age.11Sorensen O, Percy D, Dales S. In vivo and in vitro models of demyelinating diseases. III. JHM virus infection of rats. Arch Neurol 1980; 37: 478-84. Two types of studies were conducted to ascertain the involvement of the cellular immune system in development of resistance. Immunosuppression of WL rats with cyclosporin A (CsA) following onset of the age-related resistance demonstrated that this drug was partially able to abrogate resistance. In the other studies nude (rnu/rnu) rats, their heterozygous (rnu/+) litter mates and genetically related LE rats of various ages were challenged with JHMV. The rnu/+ and LE animals became completely resistant before the age of weaning, whereas some rnu/rnu rats, challenged as late as 70 days of age, showed disease symptoms—albeit after a long latent period. These observations indicated that the cellular immune system plays an important role in suppressing the disease process in the CNS. When the infection of nude rats was initiated on or after the 15th day of life, the histological lesions were generally small and present in both grey and white matter but were seldom seen in the spinal cord. Mononuclear infiltrates were evident throughout the CNS. In some nude rats there was massive mononuclear cell infiltration towards the meningies and into ventricular spaces. By contrast in rnu/+, LE and WL rats with late-onset disease symptoms, demyelinating-type lesions were confined to the white matter and only minor infiltration of mononuclear cells was evident. JHMV RNA was detectable by dot-blotting analysis in the CNS of both paralysed and asymptomatic rnu/rnu and rnu/+ rats, but less RNA was usually detected in heterozygous animals. In-situ hybridization with cDNA probes for JHMV RNA showed that neurons in the hippocampus and cerebellum, as well as cells in the white matter, were frequently infected. The present data indicate that in the rat T cells have an important function in maintaining resistance to the JHMV related disease process. However, even without a functional T cell compartment nude rats challenged after 15 days of age did not develop an acute encephalitis, suggesting that an age-dependent, non-immunological mechanism is also involved in restricting the spread of infection. It is possible that resistance in euthymic rats sets in because: (1) at the time of weaning the CNS matures, so that the number of targets available for infection is reduced, (2) T cells prevent the late-onset disease by clearing persistent, low grade infections from the CNS.</abstract><note>Supported by grants from the MS Society of Canada and the MRC of Canada.</note><note type="content">Section title: Article</note><subject><genre>Keywords</genre><topic>nude rats</topic><topic>coronavirus</topic><topic>CNS disease</topic><topic>demyelination</topic></subject><relatedItem type="host"><titleInfo><title>Microbial Pathogenesis</title></titleInfo><titleInfo type="abbreviated"><title>YMPAT</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">1987</dateIssued></originInfo><identifier type="ISSN">0882-4010</identifier><identifier type="PII">S0882-4010(00)X0196-9</identifier><part><date>1987</date><detail type="volume"><number>2</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>79</start><end>158</end></extent><extent unit="pages"><start>79</start><end>90</end></extent></part></relatedItem><identifier type="istex">8AA99663F1B420905279642F839412D56765E817</identifier><identifier type="ark">ark:/67375/6H6-LH37PTBP-9</identifier><identifier type="DOI">10.1016/0882-4010(87)90100-8</identifier><identifier type="PII">0882-4010(87)90100-8</identifier><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></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-LH37PTBP-9/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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