Primary demyelination in experimental canine distemper virus induced encephalomyelitis in gnotobiotic dogs
Identifieur interne : 000579 ( Istex/Corpus ); précédent : 000578; suivant : 000580Primary demyelination in experimental canine distemper virus induced encephalomyelitis in gnotobiotic dogs
Auteurs : R. J. Higgins ; S. G. Krakowka ; A. E. Metzler ; A. KoestnerSource :
- Acta Neuropathologica [ 0001-6322 ] ; 1982-03-01.
English descriptors
- KwdEn :
- Teeft :
- Acta, Acta neuropathol, Adjacent myelinated axons, Astrocyte, Astrocytic cell processes, Axon, Berl, Blood vessels, Canine, Canine distemper, Canine distemper virus, Canine distemper virus infection, Cell cuffing, Cell processes, Cerebellar cortex, Cerebral cortex, Cerebrospinal fluid, Choroid, Choroid plexus, Clinical signs, Demyelinated, Demyelinated axons, Demyelinating, Demyelinating encephalomyelitis, Demyelinating lesions, Demyelination, Direct injury, Distemper, Distemper encephalomyelitis, Distemper virus, Encephalomyelitis, Ependymal, Ependymal cells, Ependymal epithelium, Epithelial cells, Experimental demyelinating encephalomyelitis, Experimental infection, Fourth ventricle, Glial filaments, Gnotobiotic, Gnotobiotic dogs, Granular debris, Grey matter, Higgins, High incidence, Histologic lesions, Hypertrophic astrocytes, Immune mechanisms, Immunoglobulin, Immunoglobulin deposits, Immunologic studies, Inclusion bodies, Intact axons, Intact myelin, Intact myelinated axons, Koestner, Krakowka, Lesion, Light microscopy, Macrophage, Major role, Medulla oblongata, Mononuclear cells, Myelin, Myelin injury, Myelin lamellae, Myelin sheath, Myelinated, Myelinated axons, Neonatal gnotobiotic dogs, Neurologic signs, Neuropathol, Oligodendroglia, Other sites, Phagocytic cells, Plexus, Potential usefulness, Predilection sites, Primary demyelination, Reactive astrocytes, Remyelination, Rostral medullary velum, Routine techniques, Segmental internodal, Sequential, Spinal cord, Subependymal foci, Temporal cortex, Uniform thickness, Viral, Viral antigen, White matter.
Abstract
Summary: Experimental infection of gnotobiotic Beagle dogs at 21 days of age with neurovirulent R252 strain of canine distemper virus (R252-CDV) resulted in a non-suppurative encephalomyelitis. Segmental internodal primary demyelination was found in almost 90% of the dogs from 27 days post inoculation (DPI). Ultrastructurally demyelination was initiated by the insertion of CDV-infected astrocytic processes at nodes of Ranvier with subsequent cleavage of well-preserved myelin from the axolemma. CDV-infected macrophages were consistently involved in myelin phagocytosis. Some remyelination of denuded axons occurred after 35 DPI. Persistent productive infection of the choroid plexus and ependyma in the fourth ventricle was consistently associated with subependymal foci of demyelination. Primary demyelination occurred without detectable CDV-specific virus-neutralizing (CDV-VN) antibody in either serum or cerebrospinal fluid (CSF). There were no immunoglobulin deposits or inflammatory cells within the lesions. These findings indicate that both direct CDV antibody-dependent and CDV antibody-dependent cell-mediated immune mechanisms of cytolysis or myelin destruction are not involved in the genesis of initial primary demyelination. The sequential morphologic and serologic findings in this model of demyelinating encephalomyelitis indicate that direct virus-induced injury has a major role in both the initiation and early progression of primary demyelination.
Url:
DOI: 10.1007/BF00692691
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ISTEX:9FC873A35E2CBA3D2794F685810998BBD7B42550Le document en format XML
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Higgins</name><affiliation><mods:affiliation>Institut für vergleichende Neurologie, Universität Bern, CH-3001, Bern, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Krakowka, S G" sort="Krakowka, S G" uniqKey="Krakowka S" first="S. G." last="Krakowka">S. G. Krakowka</name><affiliation><mods:affiliation>Dept. of Veterinary Pathobiology, College of Veterinary Medicine, The Ohio State University, 43210, Columbus, OH, USA</mods:affiliation></affiliation></author><author><name sortKey="Metzler, A E" sort="Metzler, A E" uniqKey="Metzler A" first="A. E." last="Metzler">A. E. Metzler</name><affiliation><mods:affiliation>Institut für Virologie, Universität Zürich, Winterthurerstr. 266 A, CH-8057, Zürich, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Koestner, A" sort="Koestner, A" uniqKey="Koestner A" first="A." last="Koestner">A. 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Segmental internodal primary demyelination was found in almost 90% of the dogs from 27 days post inoculation (DPI). Ultrastructurally demyelination was initiated by the insertion of CDV-infected astrocytic processes at nodes of Ranvier with subsequent cleavage of well-preserved myelin from the axolemma. CDV-infected macrophages were consistently involved in myelin phagocytosis. Some remyelination of denuded axons occurred after 35 DPI. Persistent productive infection of the choroid plexus and ependyma in the fourth ventricle was consistently associated with subependymal foci of demyelination. Primary demyelination occurred without detectable CDV-specific virus-neutralizing (CDV-VN) antibody in either serum or cerebrospinal fluid (CSF). There were no immunoglobulin deposits or inflammatory cells within the lesions. These findings indicate that both direct CDV antibody-dependent and CDV antibody-dependent cell-mediated immune mechanisms of cytolysis or myelin destruction are not involved in the genesis of initial primary demyelination. The sequential morphologic and serologic findings in this model of demyelinating encephalomyelitis indicate that direct virus-induced injury has a major role in both the initiation and early progression of primary demyelination.</div></front></TEI><istex><corpusName>springer-journals</corpusName><keywords><teeft><json:string>demyelination</json:string><json:string>axon</json:string><json:string>myelin</json:string><json:string>encephalomyelitis</json:string><json:string>distemper</json:string><json:string>demyelinating</json:string><json:string>astrocyte</json:string><json:string>gnotobiotic</json:string><json:string>krakowka</json:string><json:string>koestner</json:string><json:string>myelinated</json:string><json:string>neuropathol</json:string><json:string>primary demyelination</json:string><json:string>macrophage</json:string><json:string>acta</json:string><json:string>demyelinated</json:string><json:string>immunoglobulin</json:string><json:string>plexus</json:string><json:string>berl</json:string><json:string>choroid</json:string><json:string>canine</json:string><json:string>fourth ventricle</json:string><json:string>remyelination</json:string><json:string>viral</json:string><json:string>acta neuropathol</json:string><json:string>choroid plexus</json:string><json:string>ependymal</json:string><json:string>lesion</json:string><json:string>gnotobiotic dogs</json:string><json:string>oligodendroglia</json:string><json:string>sequential</json:string><json:string>higgins</json:string><json:string>demyelinating encephalomyelitis</json:string><json:string>canine distemper virus</json:string><json:string>reactive astrocytes</json:string><json:string>spinal cord</json:string><json:string>grey matter</json:string><json:string>immune mechanisms</json:string><json:string>hypertrophic astrocytes</json:string><json:string>demyelinating lesions</json:string><json:string>demyelinated axons</json:string><json:string>granular debris</json:string><json:string>temporal cortex</json:string><json:string>medulla oblongata</json:string><json:string>blood vessels</json:string><json:string>immunoglobulin deposits</json:string><json:string>cell cuffing</json:string><json:string>canine distemper</json:string><json:string>neurologic signs</json:string><json:string>cerebral cortex</json:string><json:string>intact myelin</json:string><json:string>clinical signs</json:string><json:string>phagocytic cells</json:string><json:string>myelin sheath</json:string><json:string>experimental infection</json:string><json:string>astrocytic cell processes</json:string><json:string>glial filaments</json:string><json:string>ependymal epithelium</json:string><json:string>myelin lamellae</json:string><json:string>viral antigen</json:string><json:string>light microscopy</json:string><json:string>segmental internodal</json:string><json:string>cerebrospinal fluid</json:string><json:string>ependymal cells</json:string><json:string>white matter</json:string><json:string>distemper virus</json:string><json:string>direct injury</json:string><json:string>cerebellar cortex</json:string><json:string>major role</json:string><json:string>inclusion bodies</json:string><json:string>histologic lesions</json:string><json:string>other sites</json:string><json:string>intact myelinated axons</json:string><json:string>epithelial cells</json:string><json:string>myelinated axons</json:string><json:string>experimental demyelinating encephalomyelitis</json:string><json:string>intact axons</json:string><json:string>myelin injury</json:string><json:string>rostral medullary velum</json:string><json:string>potential usefulness</json:string><json:string>cell processes</json:string><json:string>immunologic studies</json:string><json:string>uniform thickness</json:string><json:string>canine distemper virus infection</json:string><json:string>mononuclear cells</json:string><json:string>high incidence</json:string><json:string>predilection sites</json:string><json:string>adjacent myelinated axons</json:string><json:string>neonatal gnotobiotic dogs</json:string><json:string>distemper encephalomyelitis</json:string><json:string>subependymal foci</json:string><json:string>routine techniques</json:string></teeft></keywords><author><json:item><name>R. J. Higgins</name><affiliations><json:string>Institut für vergleichende Neurologie, Universität Bern, CH-3001, Bern, Switzerland</json:string></affiliations></json:item><json:item><name>S. G. Krakowka</name><affiliations><json:string>Dept. of Veterinary Pathobiology, College of Veterinary Medicine, The Ohio State University, 43210, Columbus, OH, USA</json:string></affiliations></json:item><json:item><name>A. E. Metzler</name><affiliations><json:string>Institut für Virologie, Universität Zürich, Winterthurerstr. 266 A, CH-8057, Zürich, Switzerland</json:string></affiliations></json:item><json:item><name>A. Koestner</name><affiliations><json:string>Dept. of Pathology, Michigan State University, 48824, East Lansing, MI, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Canine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Canine distemper virus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Demyelination</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Encephalomyelitis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Antibodies</value></json:item></subject><articleId><json:string>BF00692691</json:string><json:string>Art1</json:string></articleId><arkIstex>ark:/67375/1BB-V66L2CPH-M</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>OriginalPaper</json:string></originalGenre><abstract>Summary: Experimental infection of gnotobiotic Beagle dogs at 21 days of age with neurovirulent R252 strain of canine distemper virus (R252-CDV) resulted in a non-suppurative encephalomyelitis. Segmental internodal primary demyelination was found in almost 90% of the dogs from 27 days post inoculation (DPI). Ultrastructurally demyelination was initiated by the insertion of CDV-infected astrocytic processes at nodes of Ranvier with subsequent cleavage of well-preserved myelin from the axolemma. CDV-infected macrophages were consistently involved in myelin phagocytosis. Some remyelination of denuded axons occurred after 35 DPI. Persistent productive infection of the choroid plexus and ependyma in the fourth ventricle was consistently associated with subependymal foci of demyelination. Primary demyelination occurred without detectable CDV-specific virus-neutralizing (CDV-VN) antibody in either serum or cerebrospinal fluid (CSF). There were no immunoglobulin deposits or inflammatory cells within the lesions. These findings indicate that both direct CDV antibody-dependent and CDV antibody-dependent cell-mediated immune mechanisms of cytolysis or myelin destruction are not involved in the genesis of initial primary demyelination. The sequential morphologic and serologic findings in this model of demyelinating encephalomyelitis indicate that direct virus-induced injury has a major role in both the initiation and early progression of primary demyelination.</abstract><qualityIndicators><refBibsNative>false</refBibsNative><abstractWordCount>193</abstractWordCount><abstractCharCount>1472</abstractCharCount><keywordCount>5</keywordCount><score>9.316</score><pdfWordCount>5070</pdfWordCount><pdfCharCount>29847</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>8</pdfPageCount><pdfPageSize>597.28 x 785 pts</pdfPageSize></qualityIndicators><title>Primary demyelination in experimental canine distemper virus induced encephalomyelitis in gnotobiotic dogs</title><pmid><json:string>7136512</json:string></pmid><genre><json:string>research-article</json:string></genre><host><title>Acta Neuropathologica</title><language><json:string>unknown</json:string></language><publicationDate>1982</publicationDate><copyrightDate>1982</copyrightDate><issn><json:string>0001-6322</json:string></issn><eissn><json:string>1432-0533</json:string></eissn><journalId><json:string>401</json:string></journalId><volume>58</volume><issue>1</issue><pages><first>1</first><last>8</last></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Pathology</value></json:item></subject></host><namedEntities><unitex><date></date><geogName></geogName><orgName></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName></persName><placeName></placeName><ref_url></ref_url><ref_bibl></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/1BB-V66L2CPH-M</json:string></ark><categories><wos><json:string>1 - 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pathologie infectieuse</json:string></inist></categories><publicationDate>1982</publicationDate><copyrightDate>1982</copyrightDate><doi><json:string>10.1007/BF00692691</json:string></doi><id>9FC873A35E2CBA3D2794F685810998BBD7B42550</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-V66L2CPH-M/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-V66L2CPH-M/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/1BB-V66L2CPH-M/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Primary demyelination in experimental canine distemper virus induced encephalomyelitis in gnotobiotic dogs</title><title level="a" type="sub" xml:lang="en">Sequential immunologic and morphologic findings</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><availability><licence><p>Springer-Verlag, 1982</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</p></availability><date>1982-02-23</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>Original Works</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Primary demyelination in experimental canine distemper virus induced encephalomyelitis in gnotobiotic dogs</title><title level="a" type="sub" xml:lang="en">Sequential immunologic and morphologic findings</title><author xml:id="author-0000" corresp="yes"><persName><forename type="first">R.</forename><surname>Higgins</surname></persName><affiliation>Institut für vergleichende Neurologie, Universität Bern, CH-3001, Bern, Switzerland</affiliation></author><author xml:id="author-0001"><persName><forename type="first">S.</forename><surname>Krakowka</surname></persName><affiliation>Dept. of Veterinary Pathobiology, College of Veterinary Medicine, The Ohio State University, 43210, Columbus, OH, USA</affiliation></author><author xml:id="author-0002"><persName><forename type="first">A.</forename><surname>Metzler</surname></persName><affiliation>Institut für Virologie, Universität Zürich, Winterthurerstr. 266 A, CH-8057, Zürich, Switzerland</affiliation></author><author xml:id="author-0003"><persName><forename type="first">A.</forename><surname>Koestner</surname></persName><affiliation>Dept. of Pathology, Michigan State University, 48824, East Lansing, MI, USA</affiliation></author><idno type="istex">9FC873A35E2CBA3D2794F685810998BBD7B42550</idno><idno type="ark">ark:/67375/1BB-V66L2CPH-M</idno><idno type="DOI">10.1007/BF00692691</idno><idno type="article-id">BF00692691</idno><idno type="article-id">Art1</idno></analytic><monogr><title level="j">Acta Neuropathologica</title><title level="j" type="abbrev">Acta Neuropathol</title><idno type="pISSN">0001-6322</idno><idno type="eISSN">1432-0533</idno><idno type="journal-ID">true</idno><idno type="issue-article-count">12</idno><idno type="volume-issue-count">4</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1982-03-01"></date><biblScope unit="volume">58</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="1">1</biblScope><biblScope unit="page" to="8">8</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1982-02-23</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Summary: Experimental infection of gnotobiotic Beagle dogs at 21 days of age with neurovirulent R252 strain of canine distemper virus (R252-CDV) resulted in a non-suppurative encephalomyelitis. Segmental internodal primary demyelination was found in almost 90% of the dogs from 27 days post inoculation (DPI). Ultrastructurally demyelination was initiated by the insertion of CDV-infected astrocytic processes at nodes of Ranvier with subsequent cleavage of well-preserved myelin from the axolemma. CDV-infected macrophages were consistently involved in myelin phagocytosis. Some remyelination of denuded axons occurred after 35 DPI. Persistent productive infection of the choroid plexus and ependyma in the fourth ventricle was consistently associated with subependymal foci of demyelination. Primary demyelination occurred without detectable CDV-specific virus-neutralizing (CDV-VN) antibody in either serum or cerebrospinal fluid (CSF). There were no immunoglobulin deposits or inflammatory cells within the lesions. These findings indicate that both direct CDV antibody-dependent and CDV antibody-dependent cell-mediated immune mechanisms of cytolysis or myelin destruction are not involved in the genesis of initial primary demyelination. The sequential morphologic and serologic findings in this model of demyelinating encephalomyelitis indicate that direct virus-induced injury has a major role in both the initiation and early progression of primary demyelination.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Key words</head><item><term>Canine</term></item><item><term>Canine distemper virus</term></item><item><term>Demyelination</term></item><item><term>Encephalomyelitis</term></item><item><term>Antibodies</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Pathology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1982-02-23">Created</change><change when="1982-03-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-V66L2CPH-M/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus springer-journals not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Berlin/Heidelberg</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>401</JournalID><JournalPrintISSN>0001-6322</JournalPrintISSN><JournalElectronicISSN>1432-0533</JournalElectronicISSN><JournalTitle>Acta Neuropathologica</JournalTitle><JournalAbbreviatedTitle>Acta Neuropathol</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Medicine & Public Health</JournalSubject><JournalSubject Type="Secondary">Pathology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>58</VolumeIDStart><VolumeIDEnd>58</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>1</IssueIDStart><IssueIDEnd>1</IssueIDEnd><IssueArticleCount>12</IssueArticleCount><IssueHistory><CoverDate><DateString>1982</DateString><Year>1982</Year><Month>3</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1982</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art1"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF00692691</ArticleID><ArticleDOI>10.1007/BF00692691</ArticleDOI><ArticleSequenceNumber>1</ArticleSequenceNumber><ArticleTitle Language="En">Primary demyelination in experimental canine distemper virus induced encephalomyelitis in gnotobiotic dogs</ArticleTitle><ArticleSubTitle Language="En">Sequential immunologic and morphologic findings</ArticleSubTitle><ArticleCategory>Original Works</ArticleCategory><ArticleFirstPage>1</ArticleFirstPage><ArticleLastPage>8</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2004</Year><Month>11</Month><Day>9</Day></RegistrationDate><Received><Year>1982</Year><Month>2</Month><Day>23</Day></Received><Accepted><Year>1982</Year><Month>5</Month><Day>25</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1982</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>401</JournalID><VolumeIDStart>58</VolumeIDStart><VolumeIDEnd>58</VolumeIDEnd><IssueIDStart>1</IssueIDStart><IssueIDEnd>1</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff2"><AuthorName DisplayOrder="Western"><GivenName>R.</GivenName><GivenName>J.</GivenName><FamilyName>Higgins</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>S.</GivenName><GivenName>G.</GivenName><FamilyName>Krakowka</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff4"><AuthorName DisplayOrder="Western"><GivenName>A.</GivenName><GivenName>E.</GivenName><FamilyName>Metzler</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff5"><AuthorName DisplayOrder="Western"><GivenName>A.</GivenName><FamilyName>Koestner</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Institut für vergleichende Neurologie</OrgDivision><OrgName>Universität Bern</OrgName><OrgAddress><Postcode>CH-3001</Postcode><City>Bern</City><Country>Switzerland</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Dept. of Veterinary Pathobiology, College of Veterinary Medicine</OrgDivision><OrgName>The Ohio State University</OrgName><OrgAddress><Postcode>43210</Postcode><City>Columbus</City><State>OH</State><Country>USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Institut für Virologie</OrgDivision><OrgName>Universität Zürich</OrgName><OrgAddress><Street>Winterthurerstr. 266 A</Street><Postcode>CH-8057</Postcode><City>Zürich</City><Country>Switzerland</Country></OrgAddress></Affiliation><Affiliation ID="Aff5"><OrgDivision>Dept. of Pathology</OrgDivision><OrgName>Michigan State University</OrgName><OrgAddress><Postcode>48824</Postcode><City>East Lansing</City><State>MI</State><Country>USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgAddress><Street>2300 Commonwealth Ave.</Street><Postcode>02166</Postcode><City>Newton</City><State>MA</State><Country>USA</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Experimental infection of gnotobiotic Beagle dogs at 21 days of age with neurovirulent R252 strain of canine distemper virus (R252-CDV) resulted in a non-suppurative encephalomyelitis. Segmental internodal primary demyelination was found in almost 90% of the dogs from 27 days post inoculation (DPI). Ultrastructurally demyelination was initiated by the insertion of CDV-infected astrocytic processes at nodes of Ranvier with subsequent cleavage of well-preserved myelin from the axolemma. CDV-infected macrophages were consistently involved in myelin phagocytosis. Some remyelination of denuded axons occurred after 35 DPI. Persistent productive infection of the choroid plexus and ependyma in the fourth ventricle was consistently associated with subependymal foci of demyelination.</Para><Para>Primary demyelination occurred without detectable CDV-specific virus-neutralizing (CDV-VN) antibody in either serum or cerebrospinal fluid (CSF). There were no immunoglobulin deposits or inflammatory cells within the lesions. These findings indicate that both direct CDV antibody-dependent and CDV antibody-dependent cell-mediated immune mechanisms of cytolysis or myelin destruction are not involved in the genesis of initial primary demyelination. The sequential morphologic and serologic findings in this model of demyelinating encephalomyelitis indicate that direct virus-induced injury has a major role in both the initiation and early progression of primary demyelination.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>Canine</Keyword><Keyword>Canine distemper virus</Keyword><Keyword>Demyelination</Keyword><Keyword>Encephalomyelitis</Keyword><Keyword>Antibodies</Keyword></KeywordGroup><ArticleNote Type="Misc"><SimplePara>Supported by The State of Ohio Canine Research Fund and Grant Number 2 ROI NS 14821, National Institutes of Health, USA. A.E.M. was supported by the Schweizerische Stiftung für Medizinisch-biologische Stipendien, Basel and the Janggen-Pohen-Stiftung, St. Gallen, Switzerland</SimplePara></ArticleNote></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Primary demyelination in experimental canine distemper virus induced encephalomyelitis in gnotobiotic dogs</title><subTitle>Sequential immunologic and morphologic findings</subTitle></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Primary demyelination in experimental canine distemper virus induced encephalomyelitis in gnotobiotic dogs</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">R.</namePart><namePart type="given">J.</namePart><namePart type="family">Higgins</namePart><affiliation>Institut für vergleichende Neurologie, Universität Bern, CH-3001, Bern, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="given">G.</namePart><namePart type="family">Krakowka</namePart><affiliation>Dept. of Veterinary Pathobiology, College of Veterinary Medicine, The Ohio State University, 43210, Columbus, OH, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="given">E.</namePart><namePart type="family">Metzler</namePart><affiliation>Institut für Virologie, Universität Zürich, Winterthurerstr. 266 A, CH-8057, Zürich, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Koestner</namePart><affiliation>Dept. of Pathology, Michigan State University, 48824, East Lansing, MI, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" 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>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateCreated encoding="w3cdtf">1982-02-23</dateCreated><dateIssued encoding="w3cdtf">1982-03-01</dateIssued><copyrightDate encoding="w3cdtf">1982</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Summary: Experimental infection of gnotobiotic Beagle dogs at 21 days of age with neurovirulent R252 strain of canine distemper virus (R252-CDV) resulted in a non-suppurative encephalomyelitis. Segmental internodal primary demyelination was found in almost 90% of the dogs from 27 days post inoculation (DPI). Ultrastructurally demyelination was initiated by the insertion of CDV-infected astrocytic processes at nodes of Ranvier with subsequent cleavage of well-preserved myelin from the axolemma. CDV-infected macrophages were consistently involved in myelin phagocytosis. Some remyelination of denuded axons occurred after 35 DPI. Persistent productive infection of the choroid plexus and ependyma in the fourth ventricle was consistently associated with subependymal foci of demyelination. Primary demyelination occurred without detectable CDV-specific virus-neutralizing (CDV-VN) antibody in either serum or cerebrospinal fluid (CSF). There were no immunoglobulin deposits or inflammatory cells within the lesions. These findings indicate that both direct CDV antibody-dependent and CDV antibody-dependent cell-mediated immune mechanisms of cytolysis or myelin destruction are not involved in the genesis of initial primary demyelination. The sequential morphologic and serologic findings in this model of demyelinating encephalomyelitis indicate that direct virus-induced injury has a major role in both the initiation and early progression of primary demyelination.</abstract><note>Original Works</note><subject lang="en"><genre>Key words</genre><topic>Canine</topic><topic>Canine distemper virus</topic><topic>Demyelination</topic><topic>Encephalomyelitis</topic><topic>Antibodies</topic></subject><relatedItem type="host"><titleInfo><title>Acta Neuropathologica</title></titleInfo><titleInfo type="abbreviated"><title>Acta Neuropathol</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>Springer</publisher><dateIssued encoding="w3cdtf">1982-03-01</dateIssued><copyrightDate encoding="w3cdtf">1982</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Pathology</topic></subject><identifier type="ISSN">0001-6322</identifier><identifier type="eISSN">1432-0533</identifier><identifier type="JournalID">401</identifier><identifier type="IssueArticleCount">12</identifier><identifier type="VolumeIssueCount">4</identifier><part><date>1982</date><detail type="volume"><number>58</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="pages"><start>1</start><end>8</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1982</recordOrigin></recordInfo></relatedItem><identifier type="istex">9FC873A35E2CBA3D2794F685810998BBD7B42550</identifier><identifier type="ark">ark:/67375/1BB-V66L2CPH-M</identifier><identifier type="DOI">10.1007/BF00692691</identifier><identifier type="ArticleID">BF00692691</identifier><identifier type="ArticleID">Art1</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag, 1982</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Springer-Verlag, 1982</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-V66L2CPH-M/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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