Absence of a robust innate immune response in rat neurons facilitates persistent infection of Borna disease virus in neuronal tissue.

摘要: Borna disease virus (BDV) persistently infects neurons of the central nervous system various hosts, including rats. Since type I IFN-mediated antiviral response efficiently blocks BDV replication in primary rat embryo fibroblasts, it has been speculated that is not effectively sensed by host innate immune system. To test this assumption, organotypical hippocampal slice cultures were infected with for up to 4 weeks. This resulted secretion IFN and up-regulation IFN-stimulated genes. Using Mx protein as a specific marker IFN-induced gene expression, astrocytes microglial cells found be positive, whereas neurons, major cell which replicating, lacked detectable levels protein. In uninfected cultures, also remained negative even after treatment high concentrations IFN-α. non-responsiveness correlated lack nuclear translocation both pSTAT1 pSTAT2 these cells. Consistently, neuronal dissemination was prevented These data suggest poor renders highly susceptible infection presence exogenous Intriguingly, contrast IFN-α mouse proteins block replication, indicating species-specific differences between mice