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  • 1
    Electronic Resource
    Electronic Resource
    Astrocytic infection in canine distemper virus-induced demyelination (1989)
    Springer
    Acta neuropathologica 77 (1989), S. 333-335 
    Details
    ISSN: 1432-0533
    Keywords: Canine distemper virus ; Astrocyte ; Immunocytochemistry ; Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acute canine distemper virus (CDV)-induced demyelinating lesions were examined with double-labelling immunocytochemistry simultaneously demonstrating CDV antigen and glial fibrillary acidid protein (GFAP) as marker for astrocytes. It was shown that 64% of all astrocytes within the demyelinating lesions were infected and that 95% of all infected cells counted in the lesions were astrocytes. These results suggest that the astrocyte ist the main target for CDV and that astroglial infection may play an important role in the mechanism of demyelination.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687587
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Chronic relapsing demyelinating encephalomyelitis associated with persistent spontaneous canine distemper virus infection (1989)
    Springer
    Acta neuropathologica 77 (1989), S. 441-444 
    Details
    ISSN: 1432-0533
    Keywords: Canine distemper virus ; Demyelination ; IgG index ; Encephalomyelitis ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This is the first report of spontaneous canine distemper virus (CDV) infection in a dog associated with chronic progressive multiphasic neurological disease. Initial neurological deficits in the pelvic limbs progressed rapidly to paraplegia with almost complete remission after 9 weeks. Then another acute episode occurred with severe thoracic limb deficits and cerebellar dysfunction and progressive neurological deterioration over 3 months with rising serum neutralizing (SN) anti-CDV titers in the serum and cerebrospinal fluid (CSF). Three neuropathologically distinct lesions of spinal cystic necrosis, chronic demyelinating foci in the cerebellum and acute demyelinating encephalitis in the pons were identified. Persistent CDV antigen was demonstrated immunocytochemically only in acute lesions and atypically restricted to neurons. However, the immunological mechanism associated with the distinct remissions and exacerbations and CDV antigen clearance from chronic demyelinating lesions but persistence in acute lesions, despite a vigorous anti-CDV serologic response, was not defined.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687381
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Spread and distribution of viral antigen in nervous canine distemper (1985)
    Springer
    Acta neuropathologica 67 (1985), S. 211-218 
    Details
    ISSN: 1432-0533
    Keywords: Canine distemper virus ; Demyelination ; Dog ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Canine distemper virus (CDV) antigen was demonstrated immunocytochemically in the central nervous system (CNS) of 19 dogs killed from 16 to 170 days after infection. In the earliest lesions, infection of glial cells preceded demyelination, and the degree of myelin destruction correlated with the amount of viral antigen in the tissue. It was concluded that initial demyelination in distemper is directly viral-induced, but the nature of the infected glial cells remains uncertain. Ependymal infection and spread of virus in the subependymal white matter was often seen, suggesting invasion of CDV into the CNS along the CSF pathways. Inflammation during the latter stages of the infection appeared to be associated with viral clearance from the CNS in most dogs. In two dogs with chronic progressive neurologic distemper, viral antigen was still present in the brain suggesting that viral persistence and associated immunologic reactions may contribute to further myelin damage. With the exception of one dog that survived for 6 months after infection, viral antigen was no longer detected in the dogs that had reeovered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687803
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Restricted infection with canine distemper virus leads to down-regulation of myelin gene transcription in cultured oligodendrocytes (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 312-318 
    Details
    ISSN: 1432-0533
    Keywords: Canine distemper virus ; Oligodendrocytes ; Myelin gene expression ; Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Canine distemper virus (CDV) induces oligodendroglial degeneration and multifocal demyelination in the central nervous system. The mechanism of oligodendrocyte degeneration is not understood but it has been shown that there is a restricted infection of these cells without viral protein production. Using a combination of immunocytochemistry and in situ hybridization we were able to demonstrate the transcription of the entire virus genome throughout the whole observation period (7–35 days after infection) in oligodendrocytes in CDV-infected brain cell cultures. Therefore, the lack of viral protein and particle production can not be explained on the basis of a defective viral transcription. The present study also shows that a restricted infection of oligodendrocytes with CDV down-regulates the transcription of the major myelin genes coding for proteolipid protein, myelin basic protein (MBP) and myelin-associated glycoprotein in a very similar way. Using densitometry for in situ hybridization products of MBP in populations of normal and infected oligodendrocytes, an effect could be observed long before morphological changes were detectable. The present results strongly suggest that demyelination in distemper is induced by a restricted CDV infection of oligodendrocytes which down-regulates the expression of a variety of cellular genes, in particular those coding for myelin proteins. Consequently, the infected cells are no longer able to synthesize all the membrane compounds which are necessary for maintaining their structural integrity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296516
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  • 5
    Electronic Resource
    Electronic Resource
    Canine distemper virus-immune complexes induce bystander degeneration of oligodendrocytes (1992)
    Springer
    Acta neuropathologica 83 (1992), S. 402-407 
    Details
    ISSN: 1432-0533
    Keywords: Brain cell cultures ; Bystander demyelination ; Canine distemper virus ; Oligodendrocytes ; Immune complexes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Demyelination in chronic canine distemper encephalitis may be the result of a bystander effect in which the antiviral immune response is involved. In the present report we demonstrate that canine distemper virus-antiviral antibody immune complexes induce oligodendroglial degeneration in mixed brain cell cultures, particularly at the level of the cell processes. The involvement of macrophages as effector cells in this process was confirmed by depletion of these cells from the cultures which prevented the immune complex-mediated oligodendroglial degeneration. Canine distemper virus-immune complex-induced oligodendroglial pathology is thought to be mediated by toxic factors released from stimulated macrophages. this bystander effect demonstrated here in vitro may be relevant to the mechanisms of demyelination in vivo, in which virus persistence plays an important role.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00713532
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Ultrastructural and biochemical findings in brain cell cultures infected with canine distemper virus (1990)
    Springer
    Acta neuropathologica 80 (1990), S. 59-67 
    Details
    ISSN: 1432-0533
    Keywords: Brain cell culture ; Canine distemper virus ; Cerebroside sulfotransferase ; Electron microscopy ; Oligodendrocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To study the pathomechanism of demyelination in canine distemper (CD), dog brain cell cultures were infected with virulent A75/17-CD virus (CDV) and examined ultrastructurally. Special attention was paid to the oligodendrocytes, which were specifically immunolabelled. In addition, cerebroside sulfotransferase (CST), an enzyme specific for oligodendrocyte activity was assayed during the course of the infection. Infection and maturation as well as CDV-induced changes were found in astrocytes and brain macrophages. Infection of oligodendrocytes was rarely seen, although CST activity of the culture markedly decreased and vacuolar degeneration of these cells occurred, resulting in their complete disappearance. We concluded that the degeneration of oligodendrocytes and demyelination is not due to direct virus-oligodendrocyte interaction, but due to CDV-induced events in other glial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294222
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  • 7
    Electronic Resource
    Electronic Resource
    Canine distemper virus-induced glial cell changes in vitro (1983)
    Springer
    Acta neuropathologica 62 (1983), S. 51-58 
    Details
    ISSN: 1432-0533
    Keywords: Canine distemper virus ; Brain tissue culture ; Astrocyte ; Oligodendrocyte ; Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In vitro studies on glial cell changes in canine distemper virus (CDV) infection could be useful for the understanding of the pathogenesis of demyelination in vivo in this disease. Mixed glial cell cultures derived from neonatal mice and dogs were infected with CDV and examined using immunocytochemical techniques demonstrating specific oligodendroglial and astroglial cell markers. Astrocytic changes were similar in both murine and canine cultures and consisted of loss of processes, cell fusion, and cell necrosis. Marked oligodendroglial lesions were apparent in the canine brain cultures and were characterized by focal perikaryal protrusions, swelling and loss of cell processes, and cell necrosis. Fusion between oligodendrocytes was not observed. Fusion between astrocytes and oligodendrocytes could not be documented with double labeling techniques. In contrast to the canine cultures, murine oligodendrocytes remained relatively unaffected by the infection. These findings were discussed with respect to cell pathology and mechanisms of demyelination in vivo. The exact nature of the canine oligodendroglial lesions in vitro needs to be studied in further experiments.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00684920
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  • 8
    Electronic Resource
    Electronic Resource
    Oligodendroglial pathology in canine distemper virus infection in vitro (1987)
    Springer
    Acta neuropathologica 74 (1987), S. 366-373 
    Details
    ISSN: 1432-0533
    Keywords: Canine distemper virus ; Demyelination ; Oligodendrocytes ; Tissue culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Dog brain cell cultures were infected with different canine distemper virus (CDV) strains to study the oligodendrocytes, which were characterized with eight different antibodies to cover the whole oligodendroglial population in the culture. A few weeks after infection all oligodendroglial cell types started to degenerate and disappeared from the culture. However, since no CDV protein could be demonstrated in the degenerating oligodendrocytes with extensive double-labelling studies, this lesion can not be explained as being a result of cytolytic infection. This conclusion was further supported in experiments with plaque-forming CDV, in which viral replication is restricted to the cytolytic areas only; oligodendrocytes also degenerated in virus-free areas between the plaques. The hypothesis of toxic factors released by other infected cell types in the culture leading to secondary damage of the oligodendrocyte could not be confirmed by transferring supernatants from infected to normal cultures. Whereas the presence of toxic factors can not be completely excluded, the possibility of an abortive infection of the oligodendrocytes with no or very limited viral protein synthesis is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687214
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