Demyelination in experimental canine distemper virus infection: Immunological, pathologic, and immunohistological studies View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1982-12

AUTHORS

M. Vandevelde, R. J. Higgins, B. Kristensen, F. Kristensen, A. J. Steck, U. Kihm

ABSTRACT

White matter lesions were induced in the brains of eight of nine dogs by means of experimental canine distemper virus (CDV) infection. Dogs were killed at 21, 24, 31, and 42 days after infection. Lymphocyte responsiveness to Con A and PHA stimulation in vitro was severely suppressed up to 31 days post infection (p.i.), followed by partial recovery as tested at 42 days p.i. Anti-CDV neutralizing antibody response was very weak in most dogs. There was a weak increase in antimyelin and antimyelin basic protein antibodies in most dogs during the course of the experiment. Dogs killed up to 31 days p.i. developed non-inflammatory demyclinating lesions in which no immunoglobulin could be detected. One of the three dogs that were killed at 42 days p.i. developed severe inflammatory demyelination. This was the only dog with a strong anti-MBP antibody response in the CSF and immunoglobulin demonstrated in demyelinating lesions. The present study supports previous observations that demyelination in acute CDV infection is not an immune mediated lesion but that these lesions may progress as a result of the local immune response. It is uncertain at this stage whether the local immune reaction specifically causes myelin destruction or whether bystander demyelination occurs in chronic CDE. More... »

PAGES

285-293

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf00691260

DOI

http://dx.doi.org/10.1007/bf00691260

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1044659268

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/7090737


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46 schema:description White matter lesions were induced in the brains of eight of nine dogs by means of experimental canine distemper virus (CDV) infection. Dogs were killed at 21, 24, 31, and 42 days after infection. Lymphocyte responsiveness to Con A and PHA stimulation in vitro was severely suppressed up to 31 days post infection (p.i.), followed by partial recovery as tested at 42 days p.i. Anti-CDV neutralizing antibody response was very weak in most dogs. There was a weak increase in antimyelin and antimyelin basic protein antibodies in most dogs during the course of the experiment. Dogs killed up to 31 days p.i. developed non-inflammatory demyclinating lesions in which no immunoglobulin could be detected. One of the three dogs that were killed at 42 days p.i. developed severe inflammatory demyelination. This was the only dog with a strong anti-MBP antibody response in the CSF and immunoglobulin demonstrated in demyelinating lesions. The present study supports previous observations that demyelination in acute CDV infection is not an immune mediated lesion but that these lesions may progress as a result of the local immune response. It is uncertain at this stage whether the local immune reaction specifically causes myelin destruction or whether bystander demyelination occurs in chronic CDE.
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