Abstract
Borna disease (BD) has been described as an infectious progressive type of nonpurulent encephalomyelitis in horses and sheep (Nicolau and Galloway 1928; Seifried and Spatz 1930; Zwickgt 1939; Gosztonyi; and Ludwig 1984b; Ludwig et al. 1985). It is known to occur sporadically in endemic areas in Central Europe (mainly Eastern and Southern Germany) (Zwick 1939; Dürrwald 1993). In a broad variety of species, from chicken to nonhuman primates, inoculation of brain homogenates from infected animals results in clinical manifestations that range from acute fatal neurologic disease to chronic subtle neurobehavioral syndromes (Ludwig et al. 1985, 1988). Immune-mediated mechanisms (leading to inflammatory lesions) have been shown to play a major role during the development of natural (Gosztonyi and Ludwig 1984b) and experimental disease (rat) (Hirano et al. 1983; Narayan et al. 1983 a, b; Richt et al. 1989, 1990; Stitz et al. 1989). In several species, including the newborn rat (Hirano et al. 1983; Narayan et al. 1983a), the mouse (Kao et al. 1984), and the hamster (Anzil et al. 1973; Ludwig et al. 1993), persistent infection has been established that presents as learning deficiencies (Bode et al. 1989; Dittrich et al. 1989). Inapparent or subtle clinical courses have also been observed in naturally infected horses (Ihlenburg and Brehmer 1964; Lange et al. 1987; Ludwig et al., unpublished) and sheep (Matthias 1954). The broad host range and variable clinical presentations led to consideration of the possibility that humans might be infected with BDV (Amsterdam et al. 1987).
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Bode, L. (1995). Human Infections with Borna Disease Virus and Potential Pathogenic Implications. In: Koprowski, H., Lipkin, W.I. (eds) Borna Disease. Current Topics in Microbiology and Immunology, vol 190. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-78618-1_7
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