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Immunophenotypical characterization of monocytes in canine distemper virus infection
Veronika M Stein1, Nicole M S Schreiner, Peter F Moore
1Department of Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover, Bischofsholer Damm 15, D-30173 Hannover, Germany. Veronika.Stein@tiho-hannover.de
Insights
Canine distemper virus (CDV) infection impacts peripheral monocytes, enhancing immune functions like antigen presentation. This may aid viral clearance but could also worsen demyelination in the central nervous system (CNS).
Area of Science:
- Veterinary Neurology
- Immunology
- Virology
Background:
- Canine distemper virus (CDV) infection is known to cause multifocal demyelination in the central nervous system (CNS).
- Microglia and infiltrating monocytes are suspected to play a key role in the demyelination process during CDV infection.
Purpose of the Study:
- To investigate the immunophenotypic changes in peripheral monocytes during experimental CDV infection in dogs.
- To evaluate the role of peripheral monocytes in the demyelination associated with CDV infection.
Main Methods:
- Experimental CDV infection was induced in dogs.
- Peripheral blood monocytes were analyzed using flow cytometry to characterize their immunophenotype throughout the infection course.
- Expression levels of various surface molecules were quantified.
Main Results:
- Dogs developing demyelinating lesions showed the highest numbers of CDV-infected monocytes.
- Significant up-regulation of surface molecules crucial for immune response, including CD1c, B7-1, B7-2, MHC I, and CD11b, was observed.
- Peak expression of these molecules occurred 4-5 weeks post-infection, irrespective of the clinical outcome.
Conclusions:
- CDV infection in vivo enhances functions of peripheral monocytes, potentially improving viral clearance.
- Enhanced monocyte functions may also contribute to increased demyelination via a bystander effect in dogs with high CNS viral loads.
Abstract:
Canine distemper virus (CDV) infection induces multifocal demyelination in the central nervous system (CNS). It is thought that the resident macrophages of the CNS, the microglia, as well as invading monocytes associated with the inflammatory reaction may play a central role in the demyelinating process. To evaluate changes in peripheral monocytes in CDV infection their immunophenotype was characterized by flow cytometry during the course of an experimental CDV infection in dogs. The highest number of CDV-infected monocytes was found in dogs developing demyelinating lesions. In CD18, CD45, CD44, and CD14 neither up- nor down-regulation was observed. Marked up-regulation occurred in a number of surface molecules including CD1c, B7-1 and B7-2, MHC I, and CD11b. Peak expression was found at 4-5 weeks post-infection (PI), regardless of clinical outcome. All these molecules play an important role in the host's immune response, notably antigen presentation and cell adhesion. These results demonstrate that CDV infection in vivo may enhance several macrophage functions. This could lead to more effective clearance of the virus but may also increase demyelination through a bystander effect in animals that accumulated significant amounts of CDV in the CNS.
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