Tags

Type your tag names separated by a space and hit enter

Restricted canine distemper virus infection of oligodendrocytes.
Lab Invest. 1993 Mar; 68(3):277-84.LI

Abstract

BACKGROUND

Canine distemper virus, a morbillivirus induces multifocal demyelination in the central nervous system. The acute demyelination correlates with virus replication in brain cells, especially astrocytes. Observations in vivo and in vitro demonstrated degeneration of oligodendrocytes, the myelin producing cells. However, the mechanism of oligodendroglial degeneration in distemper remained unexplained. Infection of the myelin producing cells, the most obvious explanation for the phenomenon of demyelination, could not be supported by extensive searches for viral particles or antigens in these cells neither in vivo nor in vitro.

EXPERIMENTAL DESIGN

In the present study, we combined in situ hybridization to visualize viral nucleic acid sequences with immunofluorescence for oligodendroglial antigens.

RESULTS

The nonradioactive in situ hybridization technique in combination with contrast enhanced video microscopy allowed us to unequivocally demonstrate the presence of canine distemper virus nucleic acid sequences in cultured oligodendrocytes. Many oligodendrocytes close to infected foci in the brain cell cultures were found to contain viral nucleic acid sequences. Only 1% of the viral nucleic acid sequences containing oligodendrocytes also contained viral antigen. Canine distemper virus replication in these cells is clearly restricted.

CONCLUSIONS

Different possibilities why oligodendrocytes do not support a productive virus infection and mechanisms by which such a restricted infection leads to oligodendroglial degeneration and ensuing demyelination are discussed. While our results have advanced our understanding of the pathogenesis of acute demyelination in distemper, they may also offer a possible explanation for the chronic progressive or even relapsing course of the disease. A restricted infection of the oligodendrocytes may be the mechanism by which canine distemper virus persists in the central nervous system. Virus persistence is probably a key event in many chronic viral induced inflammatory demyelinating diseases.

Authors+Show Affiliations

Department of Animal Neurology, University of Berne, Switzerland.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8450647

Citation

Zurbriggen, A, et al. "Restricted Canine Distemper Virus Infection of Oligodendrocytes." Laboratory Investigation; a Journal of Technical Methods and Pathology, vol. 68, no. 3, 1993, pp. 277-84.
Zurbriggen A, Yamawaki M, Vandevelde M. Restricted canine distemper virus infection of oligodendrocytes. Lab Invest. 1993;68(3):277-84.
Zurbriggen, A., Yamawaki, M., & Vandevelde, M. (1993). Restricted canine distemper virus infection of oligodendrocytes. Laboratory Investigation; a Journal of Technical Methods and Pathology, 68(3), 277-84.
Zurbriggen A, Yamawaki M, Vandevelde M. Restricted Canine Distemper Virus Infection of Oligodendrocytes. Lab Invest. 1993;68(3):277-84. PubMed PMID: 8450647.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Restricted canine distemper virus infection of oligodendrocytes. AU - Zurbriggen,A, AU - Yamawaki,M, AU - Vandevelde,M, PY - 1993/3/1/pubmed PY - 1993/3/1/medline PY - 1993/3/1/entrez SP - 277 EP - 84 JF - Laboratory investigation; a journal of technical methods and pathology JO - Lab. Invest. VL - 68 IS - 3 N2 - BACKGROUND: Canine distemper virus, a morbillivirus induces multifocal demyelination in the central nervous system. The acute demyelination correlates with virus replication in brain cells, especially astrocytes. Observations in vivo and in vitro demonstrated degeneration of oligodendrocytes, the myelin producing cells. However, the mechanism of oligodendroglial degeneration in distemper remained unexplained. Infection of the myelin producing cells, the most obvious explanation for the phenomenon of demyelination, could not be supported by extensive searches for viral particles or antigens in these cells neither in vivo nor in vitro. EXPERIMENTAL DESIGN: In the present study, we combined in situ hybridization to visualize viral nucleic acid sequences with immunofluorescence for oligodendroglial antigens. RESULTS: The nonradioactive in situ hybridization technique in combination with contrast enhanced video microscopy allowed us to unequivocally demonstrate the presence of canine distemper virus nucleic acid sequences in cultured oligodendrocytes. Many oligodendrocytes close to infected foci in the brain cell cultures were found to contain viral nucleic acid sequences. Only 1% of the viral nucleic acid sequences containing oligodendrocytes also contained viral antigen. Canine distemper virus replication in these cells is clearly restricted. CONCLUSIONS: Different possibilities why oligodendrocytes do not support a productive virus infection and mechanisms by which such a restricted infection leads to oligodendroglial degeneration and ensuing demyelination are discussed. While our results have advanced our understanding of the pathogenesis of acute demyelination in distemper, they may also offer a possible explanation for the chronic progressive or even relapsing course of the disease. A restricted infection of the oligodendrocytes may be the mechanism by which canine distemper virus persists in the central nervous system. Virus persistence is probably a key event in many chronic viral induced inflammatory demyelinating diseases. SN - 0023-6837 UR - https://www.unboundmedicine.com/medline/citation/8450647/Restricted_canine_distemper_virus_infection_of_oligodendrocytes_ DB - PRIME DP - Unbound Medicine ER -