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Demyelinating encephalomyelitis induced by a long-term corona virus infection in rats

Identifieur interne : 001E96 ( Main/Exploration ); précédent : 001E95; suivant : 001E97

Demyelinating encephalomyelitis induced by a long-term corona virus infection in rats

Auteurs : K. Nagashima [Allemagne] ; H. Wege [Allemagne] ; R. Meyermann [Allemagne] ; V. Ter Meulen [Allemagne]

Source :

RBID : ISTEX:893A3708A5B07785EA0E3694B68A9E8274262348

Descripteurs français

English descriptors

Abstract

Summary: 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.

Url:
DOI: 10.1007/BF00702672


Affiliations:


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<div type="abstract" xml:lang="en">Summary: 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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