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Neonatal Borna disease virus infection in Lewis rats causes targeted neuropathology linked to microglial activation and selective neuronal apoptosis in the dentate gyrus, cerebellum, and neocortex.
In neonatal Lewis rats infected with Borna disease virus, targeted pathogenesis is linked to microglial activation and specific neuronal apoptosis rather than viral tropism.
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Microglial activation may drive selective apoptosis in neonatal viral models; leaves open translation to human neurodevelopmental disorders.
Lewis rats neonatally infected with Borna disease virus have a behavioral syndrome characterized by hyperactivity, movement disorders, and abnormal social interactions. Virus is widely distributed in brain; however, neuropathology is focused in dentate gyrus, cerebellum, and neocortex where granule cells, Purkinje cells and pyramidal cells are lost through apoptosis. Although a transient immune response is present, its distribution does not correlate with sites of damage. Neuropathology is instead colocalized with microglial proliferation and expression of MHC class I and class II, ICAM, CD4 and CD8 molecules. Targeted pathogenesis in this system appears to be linked to microglial activation and susceptibility of specific neuronal populations to apoptosis rather than viral tropism or virus-specific immune responses.
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Weißenböck et al. (2000) studied Borna disease virus infection. Borna disease virus (BDV) strain He/80-1 vs. Phosphate-buffered saline (PBS) was evaluated on Neuropathology and neuronal apoptosis. Neonatal Borna disease virus infection in Lewis rats causes targeted neuropathology linked to microglial activation and selective neuronal apoptosis in the dentate gyrus, cerebellum, and neocortex.
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