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Viruses 2014, 6(7), 2571-2601; doi:10.3390/v6072571

New Aspects of the Pathogenesis of Canine Distemper Leukoencephalitis

1
Department of Pathology, University of Veterinary Medicine, Bünteweg 17, Hannover D-30559, Germany
2
Department of Pathology, Faculty of Veterinary Science, Chulalongkorn University, Bangkok 10330, Thailand
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 26 March 2014 / Revised: 11 June 2014 / Accepted: 17 June 2014 / Published: 2 July 2014
(This article belongs to the Special Issue Morbillivirus Infections)
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Abstract

Canine distemper virus (CDV) is a member of the genus morbillivirus, which is known to cause a variety of disorders in dogs including demyelinating leukoencephalitis (CDV-DL). In recent years, substantial progress in understanding the pathogenetic mechanisms of CDV-DL has been made. In vivo and in vitro investigations provided new insights into its pathogenesis with special emphasis on axon-myelin-glia interaction, potential endogenous mechanisms of regeneration, and astroglial plasticity. CDV-DL is characterized by lesions with a variable degree of demyelination and mononuclear inflammation accompanied by a dysregulated orchestration of cytokines as well as matrix metalloproteinases and their inhibitors. Despite decades of research, several new aspects of the neuropathogenesis of CDV-DL have been described only recently. Early axonal damage seems to represent an initial and progressive lesion in CDV-DL, which interestingly precedes demyelination. Axonopathy may, thus, function as a potential trigger for subsequent disturbed axon-myelin-glia interactions. In particular, the detection of early axonal damage suggests that demyelination is at least in part a secondary event in CDV-DL, thus challenging the dogma of CDV as a purely primary demyelinating disease. Another unexpected finding refers to the appearance of p75 neurotrophin (NTR)-positive bipolar cells during CDV-DL. As p75NTR is a prototype marker for immature Schwann cells, this finding suggests that Schwann cell remyelination might represent a so far underestimated endogenous mechanism of regeneration, though this hypothesis still remains to be proven. Although it is well known that astrocytes represent the major target of CDV infection in CDV-DL, the detection of infected vimentin-positive astrocytes in chronic lesions indicates a crucial role of this cell population in nervous distemper. While glial fibrillary acidic protein represents the characteristic intermediate filament of mature astrocytes, expression of vimentin is generally restricted to immature or reactive astrocytes. Thus, vimentin-positive astrocytes might constitute an important cell population for CDV persistence and spread, as well as lesion progression. In vitro models, such as dissociated glial cell cultures, as well as organotypic brain slice cultures have contributed to a better insight into mechanisms of infection and certain morphological and molecular aspects of CDV-DL. Summarized, recent in vivo and in vitro studies revealed remarkable new aspects of nervous distemper. These new perceptions substantially improved our understanding of the pathogenesis of CDV-DL and might represent new starting points to develop novel treatment strategies. View Full-Text
Keywords: axon; canine distemper virus; central nervous system; cytokine; distemper leukoencephalitis; immature astrocyte; matrix metalloproteinase; p75 neurotrophin receptor; Schwann cell; vimentin axon; canine distemper virus; central nervous system; cytokine; distemper leukoencephalitis; immature astrocyte; matrix metalloproteinase; p75 neurotrophin receptor; Schwann cell; vimentin
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MDPI and ACS Style

Lempp, C.; Spitzbarth, I.; Puff, C.; Cana, A.; Kegler, K.; Techangamsuwan, S.; Baumgärtner, W.; Seehusen, F. New Aspects of the Pathogenesis of Canine Distemper Leukoencephalitis. Viruses 2014, 6, 2571-2601.

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