[Frontiers in Bioscience 7, d541-555, Feburary 1, 2002]

THE IMMUNOPATHOGENESIS OF BORNA DISEASE VIRUS INFECTION

Lothar Stitz1, Thomas Bilzer2, and Oliver Planz1

1Institute for Immunology, Federal Research Center for Virus Diseases of Animals, Paul-Ehrlich-Strasse 28, D-72076 Tübingen, FRG, and 2Institute for Neuropathology, Heinrich-Heine-Universität, Düsseldorf, FRG.

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Dissemination of Borna Disease Virus
4. Dissemination of immune cells in Borna Disease
5. Immunopathology in Borna Disease
5.1 Evidence for the role of CD8-positive T cells
5.2 Role of CD4-positive T cells in Borna Disease Virus immunopathogenesis
5.3 Modulating and direct effects of locally synthesized molecules
5.4 CD8-positive cytotoxic T lymphocytes as effector cells in Borna disease
6. Acknowledgements
7. References

1. ABSTRACT

Borna disease virus (BDV) infection represents an excellent model system to study immunopathological mechanisms based on a T cell-mediated immune reaction in the central nervous system. The single-stranded RNA Borna disease virus, a member of Bornaviridae in the order of Mononegavirale, lacks cytopathogenicity both in vitro and in vivo. After experimental infection BDV causes a persistent infection of the central nervous system and induces Borna disease, an immune-mediated encephalomyelitis. The infiltrating immune cells have been characterized as CD4-positive, CD8-positive T-cells, macrophages and B cells. CD8-positive T cells represent the effector cell population exhibiting antigen specificity for the nucleoprotein.