Demyelinating encephalomyelitis induced by a long-term corona virus infection in rats. A preliminary report.
Identifieur interne : 001764 ( Main/Merge ); précédent : 001763; suivant : 001765Demyelinating encephalomyelitis induced by a long-term corona virus infection in rats. A preliminary report.
Auteurs : K. Nagashima ; H. Wege ; R. Meyermann ; V. Ter MeulenSource :
- Acta neuropathologica [ 0001-6322 ] ; 1979.
Descripteurs français
- KwdFr :
- MESH :
- analyse : Antigènes viraux.
- étiologie : Encéphalomyélite, Maladies démyélinisantes.
- Animaux, Facteurs temps, Infections à Coronaviridae, Maladie chronique, Rats, Récidive.
English descriptors
- KwdEn :
- MESH :
- chemical , analysis : Antigens, Viral.
- complications : Coronaviridae Infections.
- etiology : Demyelinating Diseases, Encephalomyelitis.
- Animals, Chronic Disease, Rats, Recurrence, Time Factors.
Abstract
About 30% of weanling rats inoculated with JHM virus developed a subacute demyelinating encephalomyelitis (SDE) 3 weeks after inoculation (a.i.). From the remaining animals, 5% displayed overt neurological signs 3, 6, and 8 months a.i. Animals with and without clinical signs 6-8 months a.i. were morphologically examined. Fresh demyelinating lesions could be demonstrated in paralyzed animals. Viral antigen was demonstrated and infectious JHM virus could be recovered from one animal which developed clinical signs at 3 months a.i. In one animal with clinical onset of 8 months a.i. completely remyelinated areas as well as recent demyelinating lesions were observed, suggesting a recurrence of the disease process. Remyelinated areas were also found in 40% of clinically silent animals. The morphology of the late onset of the demyelination was similar to that occurring in SDE. Remyelination consisted of both CNS and PNS-type. This animal model offers the possibility to investigate the virus-host relationship which is responsible for the induction of a demyelinating process after a long incubation period.
DOI: 10.1007/bf00702672
PubMed: 220834
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pubmed:220834Le document en format XML
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<author><name sortKey="Meyermann, R" sort="Meyermann, R" uniqKey="Meyermann R" first="R" last="Meyermann">R. Meyermann</name>
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<author><name sortKey="Ter Meulen, V" sort="Ter Meulen, V" uniqKey="Ter Meulen V" first="V" last="Ter Meulen">V. Ter Meulen</name>
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<term>Antigens, Viral (analysis)</term>
<term>Chronic Disease</term>
<term>Coronaviridae Infections (complications)</term>
<term>Demyelinating Diseases (etiology)</term>
<term>Encephalomyelitis (etiology)</term>
<term>Rats</term>
<term>Recurrence</term>
<term>Time Factors</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Antigènes viraux (analyse)</term>
<term>Encéphalomyélite (étiologie)</term>
<term>Facteurs temps</term>
<term>Infections à Coronaviridae ()</term>
<term>Maladie chronique</term>
<term>Maladies démyélinisantes (étiologie)</term>
<term>Rats</term>
<term>Récidive</term>
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<keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Antigens, Viral</term>
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<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Coronaviridae Infections</term>
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<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Demyelinating Diseases</term>
<term>Encephalomyelitis</term>
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<term>Maladies démyélinisantes</term>
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<term>Chronic Disease</term>
<term>Rats</term>
<term>Recurrence</term>
<term>Time Factors</term>
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<term>Facteurs temps</term>
<term>Infections à Coronaviridae</term>
<term>Maladie chronique</term>
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<front><div type="abstract" xml:lang="en">About 30% of weanling rats inoculated with JHM virus developed a subacute demyelinating encephalomyelitis (SDE) 3 weeks after inoculation (a.i.). From the remaining animals, 5% displayed overt neurological signs 3, 6, and 8 months a.i. Animals with and without clinical signs 6-8 months a.i. were morphologically examined. Fresh demyelinating lesions could be demonstrated in paralyzed animals. Viral antigen was demonstrated and infectious JHM virus could be recovered from one animal which developed clinical signs at 3 months a.i. In one animal with clinical onset of 8 months a.i. completely remyelinated areas as well as recent demyelinating lesions were observed, suggesting a recurrence of the disease process. Remyelinated areas were also found in 40% of clinically silent animals. The morphology of the late onset of the demyelination was similar to that occurring in SDE. Remyelination consisted of both CNS and PNS-type. This animal model offers the possibility to investigate the virus-host relationship which is responsible for the induction of a demyelinating process after a long incubation period.</div>
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