SEQUENCE OF MURINE CORONAVIRUS JHM INDUCED NEUROPATHOLOGICAL CHANGES IN RATS
Identifieur interne : 000262 ( Istex/Corpus ); précédent : 000261; suivant : 000263SEQUENCE OF MURINE CORONAVIRUS JHM INDUCED NEUROPATHOLOGICAL CHANGES IN RATS
Auteurs : M. Koga ; H. Wege ; V. Ter MeulenSource :
- Neuropathology and Applied Neurobiology [ 0305-1846 ] ; 1984-05.
English descriptors
- Teeft :
- Acta neuropathologica, Acute encephalomyelitis, Axon, Biological properties, Brain tissue, Clinical signs, Coronavirus, Demyelinated, Demyelinated foci, Demyelinated plaques, Demyelinating, Demyelinating disease, Demyelination, Demyelinative lesion, Dentate gyrus, Diseased rats, Dorsomedial part, Electron microscopy, Encephalomyelitis, Experimental medicine, General virology, Glial, Glial cells, Glial nodules, Grey matter, Hippocampal region, Infectious virus, Koga, Lampert oldstone, Lesion, Measles virus, Meulen, Meulen figure, Miles biochemicals, Murine, Murine coronavirus, Murine coronavirus strain, Mutant, Myelin, Myelin sheaths, Naked axons, Necrotic lesions, Neural parenchyma, Neural tissue, Neuron, Neuropathological, Neuropathological changes, Neutralizing, Neutralizing antibodies, Perivascular cuffs, Plaque, Plasma cells, Polymorphonuclear cells, Rat, Spinal, Spinal cord, Spinal cord tissue, Subacute, Subacute demyelinating encephalomyelitis, Target cells, Tissue culture experiments, Uranyl acetate, Viral antigen, Viral antigens, Virus, Virus antigen, Virus infection, Virus isolation, Virus particles, Virus replication, Wege, Weiner stohlman, White matter, White matter changes, Wild type.
Abstract
Infection of 21–25‐day‐old rats with the murine coronavirus JHM was followed either by an acute encephalomyelitis (AE) or subacute demyelinating encephalomyelitis (SDE). The major neuropathological finding in AE, which developed within 6–12 days pi. consisted of necrotizing lesions distributed mainly in the grey matter of the central nervous system (CNS). SDE developed 14–30 days pi. and affected rats revealed lesions of primary demyelination with predilection sites in the white matter. The time‐course for the development of lesions, virus replication and neutralizing antiviral antibody production within the first 3 weeks p.i. were studied. Within the first 2 weeks p.i., most rats showed no clinical signs but nevertheless revealed lesions typical of AE. In parallel to these neuropathological changes infectious virus could be isolated from brain and spinal cord. However, coinciding with multiplication of neutralizing JHM antibodies 10–12 days after infection no infectious virus was recoverable from CNS material. At this time many of the clinically healthy rats showed demyelinating lesions which were located at the typical predilection sites of SDE. These observations indicated that SDE was preceded by clinically silent AE lesions.
Url:
DOI: 10.1111/j.1365-2990.1984.tb00350.x
Links to Exploration step
ISTEX:4C70A9848CDD116661C5B6DEFB908A831A28B5F7Le document en format XML
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Koga</name><affiliation><mods:affiliation>Institut für Virologie und Immunbiologie der Universität Würzburg, Versbacher Strasse 7, D‐8700 Würzburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Wege, H" sort="Wege, H" uniqKey="Wege H" first="H." last="Wege">H. Wege</name><affiliation><mods:affiliation>Institut für Virologie und Immunbiologie der Universität Würzburg, Versbacher Strasse 7, D‐8700 Würzburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Meulen, V Ter" sort="Meulen, V Ter" uniqKey="Meulen V" first="V. Ter" last="Meulen">V. Ter Meulen</name><affiliation><mods:affiliation>Institut für Virologie und Immunbiologie der Universität Würzburg, Versbacher Strasse 7, D‐8700 Würzburg, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence address: †Correspondence to: V. ter Meulen.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Neuropathology and Applied Neurobiology</title><title level="j" type="alt">NEUROPATHOLOGY APPLIED NEUROBIOLOGY</title><idno type="ISSN">0305-1846</idno><idno type="eISSN">1365-2990</idno><imprint><biblScope unit="vol">10</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="173">173</biblScope><biblScope unit="page" to="184">184</biblScope><biblScope unit="page-count">12</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1984-05">1984-05</date></imprint><idno type="ISSN">0305-1846</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0305-1846</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acta neuropathologica</term><term>Acute encephalomyelitis</term><term>Axon</term><term>Biological properties</term><term>Brain tissue</term><term>Clinical signs</term><term>Coronavirus</term><term>Demyelinated</term><term>Demyelinated foci</term><term>Demyelinated plaques</term><term>Demyelinating</term><term>Demyelinating disease</term><term>Demyelination</term><term>Demyelinative lesion</term><term>Dentate gyrus</term><term>Diseased rats</term><term>Dorsomedial part</term><term>Electron microscopy</term><term>Encephalomyelitis</term><term>Experimental medicine</term><term>General virology</term><term>Glial</term><term>Glial cells</term><term>Glial nodules</term><term>Grey matter</term><term>Hippocampal region</term><term>Infectious virus</term><term>Koga</term><term>Lampert oldstone</term><term>Lesion</term><term>Measles virus</term><term>Meulen</term><term>Meulen figure</term><term>Miles biochemicals</term><term>Murine</term><term>Murine coronavirus</term><term>Murine coronavirus strain</term><term>Mutant</term><term>Myelin</term><term>Myelin sheaths</term><term>Naked axons</term><term>Necrotic lesions</term><term>Neural parenchyma</term><term>Neural tissue</term><term>Neuron</term><term>Neuropathological</term><term>Neuropathological changes</term><term>Neutralizing</term><term>Neutralizing antibodies</term><term>Perivascular cuffs</term><term>Plaque</term><term>Plasma cells</term><term>Polymorphonuclear cells</term><term>Rat</term><term>Spinal</term><term>Spinal cord</term><term>Spinal cord tissue</term><term>Subacute</term><term>Subacute demyelinating encephalomyelitis</term><term>Target cells</term><term>Tissue culture experiments</term><term>Uranyl acetate</term><term>Viral antigen</term><term>Viral antigens</term><term>Virus</term><term>Virus antigen</term><term>Virus infection</term><term>Virus isolation</term><term>Virus particles</term><term>Virus replication</term><term>Wege</term><term>Weiner stohlman</term><term>White matter</term><term>White matter changes</term><term>Wild type</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Infection of 21–25‐day‐old rats with the murine coronavirus JHM was followed either by an acute encephalomyelitis (AE) or subacute demyelinating encephalomyelitis (SDE). The major neuropathological finding in AE, which developed within 6–12 days pi. consisted of necrotizing lesions distributed mainly in the grey matter of the central nervous system (CNS). SDE developed 14–30 days pi. and affected rats revealed lesions of primary demyelination with predilection sites in the white matter. The time‐course for the development of lesions, virus replication and neutralizing antiviral antibody production within the first 3 weeks p.i. were studied. Within the first 2 weeks p.i., most rats showed no clinical signs but nevertheless revealed lesions typical of AE. In parallel to these neuropathological changes infectious virus could be isolated from brain and spinal cord. However, coinciding with multiplication of neutralizing JHM antibodies 10–12 days after infection no infectious virus was recoverable from CNS material. At this time many of the clinically healthy rats showed demyelinating lesions which were located at the typical predilection sites of SDE. 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KOGA</name><affiliations><json:string>Institut für Virologie und Immunbiologie der Universität Würzburg, Versbacher Strasse 7, D‐8700 Würzburg, Germany</json:string></affiliations></json:item><json:item><name>H. WEGE</name><affiliations><json:string>Institut für Virologie und Immunbiologie der Universität Würzburg, Versbacher Strasse 7, D‐8700 Würzburg, Germany</json:string></affiliations></json:item><json:item><name>V. TER MEULEN</name><affiliations><json:string>Institut für Virologie und Immunbiologie der Universität Würzburg, Versbacher Strasse 7, D‐8700 Würzburg, Germany</json:string><json:string>Correspondence address: †Correspondence to: V. ter Meulen.</json:string></affiliations></json:item></author><articleId><json:string>NAN173</json:string></articleId><arkIstex>ark:/67375/WNG-JQHK6G0D-H</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Infection of 21–25‐day‐old rats with the murine coronavirus JHM was followed either by an acute encephalomyelitis (AE) or subacute demyelinating encephalomyelitis (SDE). The major neuropathological finding in AE, which developed within 6–12 days pi. consisted of necrotizing lesions distributed mainly in the grey matter of the central nervous system (CNS). SDE developed 14–30 days pi. and affected rats revealed lesions of primary demyelination with predilection sites in the white matter. The time‐course for the development of lesions, virus replication and neutralizing antiviral antibody production within the first 3 weeks p.i. were studied. Within the first 2 weeks p.i., most rats showed no clinical signs but nevertheless revealed lesions typical of AE. In parallel to these neuropathological changes infectious virus could be isolated from brain and spinal cord. However, coinciding with multiplication of neutralizing JHM antibodies 10–12 days after infection no infectious virus was recoverable from CNS material. At this time many of the clinically healthy rats showed demyelinating lesions which were located at the typical predilection sites of SDE. These observations indicated that SDE was preceded by clinically silent AE lesions.</abstract><qualityIndicators><score>7.29</score><pdfWordCount>3118</pdfWordCount><pdfCharCount>20131</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>12</pdfPageCount><pdfPageSize>468 x 684 pts</pdfPageSize><pdfWordsPerPage>260</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>181</abstractWordCount><abstractCharCount>1249</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>SEQUENCE OF MURINE CORONAVIRUS JHM INDUCED NEUROPATHOLOGICAL CHANGES IN RATS</title><pmid><json:string>6330603</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Neuropathology and Applied Neurobiology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1365-2990</json:string></doi><issn><json:string>0305-1846</json:string></issn><eissn><json:string>1365-2990</json:string></eissn><publisherId><json:string>NAN</json:string></publisherId><volume>10</volume><issue>3</issue><pages><first>173</first><last>184</last><total>12</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1984</json:string></date><geogName></geogName><orgName><json:string>Johns Hopkins University</json:string><json:string>Department of Pathology, Saga Medical School Nabeshima, Saga, Japan</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Hanna Wege</json:string><json:string>Inset</json:string><json:string>Helga Kriesinger</json:string><json:string>Miles Biochemicals</json:string><json:string>Neurons</json:string><json:string>H. Wege</json:string><json:string>Margarete Sturm</json:string></persName><placeName><json:string>Germany</json:string><json:string>USA</json:string><json:string>MD</json:string><json:string>Frankfurt</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Knobler et al., 1981</json:string><json:string>Sorensen, Percy & Dales, 1980</json:string><json:string>Wege et al., 1981</json:string><json:string>Lipton & Dal Canto, 1976</json:string><json:string>Cheever et al., 1949</json:string><json:string>Joseph & Oldstone, 1975</json:string><json:string>Weiner & Stohlman, 1978</json:string><json:string>reviewed by Rima & Martin, 1976</json:string><json:string>H. Baybutt et al.</json:string><json:string>Wege et al., 1983</json:string><json:string>Nagashima et al., 1978, 1979</json:string><json:string>Knobler, Lampert & Oldstone, 1982</json:string><json:string>ter Meulen & Hall, 1978</json:string><json:string>Sorensen et al., 1982</json:string><json:string>Sternberger & Petrali, 1977</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-JQHK6G0D-H</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - pathology</json:string><json:string>2 - neurosciences</json:string><json:string>2 - clinical neurology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - neurology & neurosurgery</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Physiology (medical)</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Clinical Neurology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Neuroscience</json:string><json:string>3 - Neurology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Histology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Pathology and Forensic Medicine</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>1984</publicationDate><copyrightDate>1984</copyrightDate><doi><json:string>10.1111/j.1365-2990.1984.tb00350.x</json:string></doi><id>4C70A9848CDD116661C5B6DEFB908A831A28B5F7</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-JQHK6G0D-H/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-JQHK6G0D-H/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/WNG-JQHK6G0D-H/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">SEQUENCE OF MURINE CORONAVIRUS JHM INDUCED NEUROPATHOLOGICAL CHANGES IN RATS</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1984-05"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">SEQUENCE OF MURINE CORONAVIRUS JHM INDUCED NEUROPATHOLOGICAL CHANGES IN RATS</title><author xml:id="author-0000"><persName><forename type="first">M.</forename><surname>KOGA</surname></persName><affiliation><orgName type="institution">Institut für Virologie und Immunbiologie der Universität Würzburg</orgName><address><addrLine>Versbacher Strasse 7</addrLine><addrLine>D‐8700 Würzburg, Germany</addrLine><country key="DE" xml:lang="en">GERMANY</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">H.</forename><surname>WEGE</surname></persName><affiliation><orgName type="institution">Institut für Virologie und Immunbiologie der Universität Würzburg</orgName><address><addrLine>Versbacher Strasse 7</addrLine><addrLine>D‐8700 Würzburg, Germany</addrLine><country key="DE" xml:lang="en">GERMANY</country></address></affiliation></author><author xml:id="author-0002" role="corresp"><persName><forename type="first">V. TER</forename><surname>MEULEN</surname></persName><affiliation><orgName type="institution">Institut für Virologie und Immunbiologie der Universität Würzburg</orgName><address><addrLine>Versbacher Strasse 7</addrLine><addrLine>D‐8700 Würzburg, Germany</addrLine><country key="DE" xml:lang="en">GERMANY</country></address></affiliation></author><idno type="istex">4C70A9848CDD116661C5B6DEFB908A831A28B5F7</idno><idno type="ark">ark:/67375/WNG-JQHK6G0D-H</idno><idno type="DOI">10.1111/j.1365-2990.1984.tb00350.x</idno><idno type="unit">NAN173</idno><idno type="toTypesetVersion">file:NAN.NAN173.pdf</idno></analytic><monogr><title level="j" type="main">Neuropathology and Applied Neurobiology</title><title level="j" type="alt">NEUROPATHOLOGY APPLIED NEUROBIOLOGY</title><idno type="pISSN">0305-1846</idno><idno type="eISSN">1365-2990</idno><idno type="book-DOI">10.1111/(ISSN)1365-2990</idno><idno type="book-part-DOI">10.1111/nan.1984.10.issue-3</idno><idno type="product">NAN</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">10</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="173">173</biblScope><biblScope unit="page" to="184">184</biblScope><biblScope unit="page-count">12</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1984-05"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><encodingDesc><schemaRef type="ODD" url="https://xml-schema.delivery.istex.fr/tei-istex.odd"></schemaRef><appInfo><application ident="pub2tei" version="1.0.10" when="2019-12-20"><label>pub2TEI-ISTEX</label><desc>A set of style sheets for converting XML documents encoded in various scientific publisher formats into a common TEI format.
<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><p>Infection of 21–25‐day‐old rats with the murine coronavirus JHM was followed either by an acute encephalomyelitis (AE) or subacute demyelinating encephalomyelitis (SDE). The major neuropathological finding in AE, which developed within 6–12 days pi. consisted of necrotizing lesions distributed mainly in the grey matter of the central nervous system (CNS). SDE developed 14–30 days pi. and affected rats revealed lesions of primary demyelination with predilection sites in the white matter. The time‐course for the development of lesions, virus replication and neutralizing antiviral antibody production within the first 3 weeks p.i. were studied. Within the first 2 weeks p.i., most rats showed no clinical signs but nevertheless revealed lesions typical of AE. In parallel to these neuropathological changes infectious virus could be isolated from brain and spinal cord. However, coinciding with multiplication of neutralizing JHM antibodies 10–12 days after infection no infectious virus was recoverable from CNS material. At this time many of the clinically healthy rats showed demyelinating lesions which were located at the typical predilection sites of SDE. These observations indicated that SDE was preceded by clinically silent AE lesions.</p></abstract><textClass><keywords rend="tocHeading1"><term>Original Article</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-JQHK6G0D-H/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2990</doi><issn type="print">0305-1846</issn><issn type="electronic">1365-2990</issn><idGroup><id type="product" value="NAN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="NEUROPATHOLOGY APPLIED NEUROBIOLOGY">Neuropathology and Applied Neurobiology</title></titleGroup></publicationMeta><publicationMeta level="part" position="05003"><doi origin="wiley">10.1111/nan.1984.10.issue-3</doi><numberingGroup><numbering type="journalVolume" number="10">10</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="1984-05">May 1984</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0017300" status="forIssue"><doi origin="wiley">10.1111/j.1365-2990.1984.tb00350.x</doi><idGroup><id type="unit" value="NAN173"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="tocHeading1">Original Article</title></titleGroup><eventGroup><event type="firstOnline" date="2008-05-12"></event><event type="publishedOnlineFinalForm" date="2008-05-12"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.15 mode:FullText source:HeaderRef result:HeaderRef" date="2010-07-19"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-03"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-01"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="173">173</numbering><numbering type="pageLast" number="184">184</numbering></numberingGroup><correspondenceTo>†Correspondence to: V. ter Meulen.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NAN.NAN173.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication 29 November 1983</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="16"></count><count type="linksCrossRef" number="5"></count></countGroup><titleGroup><title type="main">SEQUENCE OF MURINE CORONAVIRUS JHM INDUCED NEUROPATHOLOGICAL CHANGES IN RATS</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" noteRef="#fn1"><personName><givenNames>M.</givenNames><familyName>KOGA</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>H.</givenNames><familyName>WEGE</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1" corresponding="yes"><personName><givenNames>V. TER</givenNames><familyName>MEULEN</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="DE"><unparsedAffiliation>Institut für Virologie und Immunbiologie der Universität Würzburg, Versbacher Strasse 7, D‐8700 Würzburg, Germany</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Infection of 21–25‐day‐old rats with the murine coronavirus JHM was followed either by an acute encephalomyelitis (AE) or subacute demyelinating encephalomyelitis (SDE). The major neuropathological finding in AE, which developed within 6–12 days pi. consisted of necrotizing lesions distributed mainly in the grey matter of the central nervous system (CNS). SDE developed 14–30 days pi. and affected rats revealed lesions of primary demyelination with predilection sites in the white matter. The time‐course for the development of lesions, virus replication and neutralizing antiviral antibody production within the first 3 weeks p.i. were studied. Within the first 2 weeks p.i., most rats showed no clinical signs but nevertheless revealed lesions typical of AE. In parallel to these neuropathological changes infectious virus could be isolated from brain and spinal cord. However, coinciding with multiplication of neutralizing JHM antibodies 10–12 days after infection no infectious virus was recoverable from CNS material. At this time many of the clinically healthy rats showed demyelinating lesions which were located at the typical predilection sites of SDE. These observations indicated that SDE was preceded by clinically silent AE lesions.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1" numbered="no"><p>*Department of Pathology, Saga Medical School Nabeshima, Saga, Japan.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>SEQUENCE OF MURINE CORONAVIRUS JHM INDUCED NEUROPATHOLOGICAL CHANGES IN RATS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>SEQUENCE OF MURINE CORONAVIRUS JHM INDUCED NEUROPATHOLOGICAL CHANGES IN RATS</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">KOGA</namePart><affiliation>Institut für Virologie und Immunbiologie der Universität Würzburg, Versbacher Strasse 7, D‐8700 Würzburg, Germany</affiliation><description>*Department of Pathology, Saga Medical School Nabeshima, Saga, Japan.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">WEGE</namePart><affiliation>Institut für Virologie und Immunbiologie der Universität Würzburg, Versbacher Strasse 7, D‐8700 Würzburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">V. TER</namePart><namePart type="family">MEULEN</namePart><affiliation>Institut für Virologie und Immunbiologie der Universität Würzburg, Versbacher Strasse 7, D‐8700 Würzburg, Germany</affiliation><affiliation>Correspondence address: †Correspondence to: V. ter Meulen.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1984-05</dateIssued><edition>Accepted for publication 29 November 1983</edition><copyrightDate encoding="w3cdtf">1984</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="references">16</extent><extent unit="linksCrossRef">5</extent></physicalDescription><abstract lang="en">Infection of 21–25‐day‐old rats with the murine coronavirus JHM was followed either by an acute encephalomyelitis (AE) or subacute demyelinating encephalomyelitis (SDE). The major neuropathological finding in AE, which developed within 6–12 days pi. consisted of necrotizing lesions distributed mainly in the grey matter of the central nervous system (CNS). SDE developed 14–30 days pi. and affected rats revealed lesions of primary demyelination with predilection sites in the white matter. The time‐course for the development of lesions, virus replication and neutralizing antiviral antibody production within the first 3 weeks p.i. were studied. Within the first 2 weeks p.i., most rats showed no clinical signs but nevertheless revealed lesions typical of AE. In parallel to these neuropathological changes infectious virus could be isolated from brain and spinal cord. However, coinciding with multiplication of neutralizing JHM antibodies 10–12 days after infection no infectious virus was recoverable from CNS material. At this time many of the clinically healthy rats showed demyelinating lesions which were located at the typical predilection sites of SDE. 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