Molecular biology of Borna disease virus.

Abstract

Originally described in the early nineteenth century as a fatal encephalitis in horses, Borna disease (BD) has become an extraordinarily valuable model for the study of both molecular mechanisms and biological consequences of persistent virus infection in the CNS (Nicolau and Galloway 1928; Zwick 1939, this volume). BD is an immune-mediated neurologic syndrome characterized by behavioral abnormalities, meningeal and parenchymal inflammatory cell infiltrates in the brain, and the accumulation of disease-specific antigen in limbic system neurons (Joest and Degen 1911; Seifried and Spatz 1930; Ludwig et al. 1988; Richt et al. 1992). As a natural infection, BD has only been confirmed to occur in horses and sheep, but experimentally it can be transmitted to an extraordinary wide range of host species, including birds, rodents and nonhuman primates (Zwick et al. 1926; Nicolau and Galloway 1928; Zwick 1939; Matthias 1954; Nitzschke 1963; Heinig 1969; Anzil et al. 1973; Ludwig et al. 1973; Metzler et al. 1976; Ludwig and Thein 1977; Sprankel et al. 1978; Stitz et al. 1980; Hirano et al. 1983, Narayan et al. 1983; Gosztonyi and Ludwig 1984; Kao et al. 1984; Ludwig et al. 1985; Waelchli et al. 1985; Richt et al. 1992). Serological data indicate that the host range may even extend to humans, although no infectious material has been isolated from human subjects (Amsterdam et al. 1985; Rott et al. 1985, 1991 ; Bode et al. 1988, 1992).