Borna disease virus (BDV) infectivity and RNA have been detected in bodily secretions and excretions, suggesting that BDV can be transmitted through salival, nasal, and conjunctival secretions and, particularly, urine and feces. BDV infection produces a range of phenotypic disease expression. BDV has a non-segmented, negative-stranded (NNS) RNA genome. Several additional viral polypeptides can be translated from spliced forms of BDV mRNAs which increases the proteomic complexity of BDV. Antibodies to both the virus G and M (gp18) proteins have neutralizing activity, suggesting that both are implicated in BDV adsorption and/or entry. Two of the BDV primary transcripts are posttranscriptionally processed by the cellular RNA splicing machinery. An intriguing aspect of the biology of BDV is the mechanism by which BDV spreads within the central nervous system (CNS). BDV appears to propagate transsynaptically, but full virus particles have never been observed at the site of synaptic junctions. These observations led to the attractive hypothesis that bare ribonucleoprotein (RNP) could be the infectious unit being transported transsynaptically within the CNS. However, recent findings have indicated that rabies virus (RV) G is absolutely required for the propagation of RV in neuronal culture cells, as well as within the mouse CNS. A section of the chapter focuses on a few selected processes to illustrate the complexity underlying the execution of the BDV gene expression program. Expression of downstream open reading frame (dORF) can be achieved by a leaky ribosome-scanning mechanism, resumption of scanning after termination of an upstream ORF, or cap-independent internal initiation.