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lüll Borna disease virus infection of adult and neonatal rats: models for neuropsychiatric disease Hornig M; Solbrig M; Horscroft N; Weissenbock H; Lipkin WICurr Top Microbiol Immunol 2001[]; 253 (ä): 157-77Animal models provide unique opportunities to explore interactions between host and environment. Two models have been established based on Borna disease virus infection that provide new insights into mechanisms by which neurotropic agents and/or immune factors may impact developing or mature CNS circuitry to effect complex disturbances in movement and behavior. Note in press: Since this chapter was submitted, several manuscripts have been published that extend findings reported here and support the relevance of BDV infections of neonatal Lewis rats as models for investigating mechanisms of neurodevelopmental damage in autism. Behavioral abnormalities, including disturbed play behavior and chronic emotional overactivity, have been described by Pletnikov et al. (1999); inhibition of responses to novel stimuli were described by Hornig et al. (1999); loss of Purkinje cells following neonatal BDV infection has been demonstrated by Eisenman et al. (1999), Hornig et al. (1999), and Weissenbock et al. (2000); and alterations in cytokine gene expression have been reported by Hornig et al. (1999), Plata-Salaman et al. (1999) and Sauder et al. (1999).|*Borna disease virus[MESH]|Animals[MESH]|Animals, Newborn[MESH]|Apoptosis[MESH]|Borna Disease/*physiopathology/virology[MESH]|Brain/growth & development/*physiopathology/virology[MESH]|Cytokines/metabolism[MESH]|Disease Models, Animal[MESH]|Encephalitis, Viral/physiopathology[MESH]|Mental Disorders/*physiopathology/virology[MESH]|Motor Activity[MESH]|Movement Disorders/physiopathology/virology[MESH]|Protein Kinase C/metabolism[MESH]|Rats[MESH]|Viral Proteins/metabolism[MESH]|Virus Latency[MESH] |