Immune cells invading the central nervous system (CNS) in response to Borna 
disease virus (BDV) antigens are central to the pathogenesis of Borna disease 
(BD). We speculate that the response of the resident cells of the brain to 
infection may be involved in the sensitization and recruitment of these 
inflammatory cells. To separate the responses of resident cells from those of 
cells infiltrating from the periphery, we used dexamethasone to inhibit 
inflammatory reactions in BD. Treatment with dexamethasone prevented the 
development of clinical signs of BD, and the brains of treated animals showed no 
neuropathological lesions and a virtual absence of markers of inflammation, cell 
infiltration, or activation normally seen in the CNS of BDV-infected rats. In 
contrast, treatment with dexamethasone exacerbated the expression of BDV RNA, 
which was paralleled by a similarly elevated expression of mRNAs for egr-1, 
c-fos, and c-jun. Furthermore, dexamethasone failed to inhibit the increase in 
expression of mRNAs for tumor necrosis factor alpha, macrophage inflammatory 
protein 1 beta, interleukin 6, and mob-1, which occurs in the CNS of animals 
infected with BDV. Our findings suggest that these genes, encoding transcription 
factors, chemokines, and proinflammatory cytokines, might be directly activated 
in CNS resident cells by BDV. This result supports the hypothesis that the 
initial phase of the inflammatory response to BDV infection in the brain may be 
dependent upon virus-induced activation of CNS resident cells.