SEQUENCE OF MURINE CORONAVIRUS JHM INDUCED NEUROPATHOLOGICAL CHANGES IN RATS
Identifieur interne : 001648 ( Main/Exploration ); précédent : 001647; suivant : 001649SEQUENCE OF MURINE CORONAVIRUS JHM INDUCED NEUROPATHOLOGICAL CHANGES IN RATS
Auteurs : M. Koga [Allemagne] ; H. Wege [Allemagne] ; V. Ter Meulen [Allemagne]Source :
- 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
Affiliations:
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Le document en format XML
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<term>Brain tissue</term>
<term>Clinical signs</term>
<term>Coronavirus</term>
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<term>Demyelinated foci</term>
<term>Demyelinated plaques</term>
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<term>Demyelinating disease</term>
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<term>Murine coronavirus</term>
<term>Murine coronavirus strain</term>
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<term>Myelin sheaths</term>
<term>Naked axons</term>
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<term>Neutralizing antibodies</term>
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<term>Plasma cells</term>
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<term>Spinal cord</term>
<term>Spinal cord tissue</term>
<term>Subacute</term>
<term>Subacute demyelinating encephalomyelitis</term>
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<term>Tissue culture experiments</term>
<term>Uranyl acetate</term>
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<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. These observations indicated that SDE was preceded by clinically silent AE lesions.</div>
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