Borna disease virus (BDV) is the prototype genus (bornavirus) of the family Bornaviridae, within the nonsegmented, negative-strand (—strand) RNA viruses (order Mononegavirales). The name Borna is derived from its association with the city of Borna, Germany, where an equine epidemic in the late 1800s crippled the Prussian cavalry. This neurotropic virus appears to be distributed worldwide and has potential to infect most, if not all, warm-blooded hosts. BDV is similar in genomic organization to other nonsegmented, (-) RNA viruses; however, its approximately 9-kb genome is smaller than those of Rhabdoviridae (about 11-15 kb), Paramyxoviridae (about 16 kb), or Filovir-idae (about 19 kb). The BDV genome is remarkably compact and encodes six major open reading frames (ORFs) in three transcription units (Fig. 1). BDV is distinctive in its nuclear localization of replication and transcription. Although this feature is shared with the plant nucleorhabdoviruses, it is unique among non-segmented, negative-strand animal RNA viruses. The first transcription unit reveals a simple pattern with only one coded protein [nucleoprotein (N), p40]. The second transcription unit encodes the proteins X (p10) and P (phosphoprotein, p23) in overlapping ORFs. The third unit contains coding sequences for the putative matrix protein (M), type I membrane

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Figure 1 BDV genomic map and transcripts. S1-S3, initiation sites of transcription; T1—T4, termination sites of transcription. Readthrough at termination signals T2 and T3 is indicated by dashed lines.

glycoprotein (G, p57, gp94), and polymerase (L, p190). Elaboration of these proteins is dependent on a variety of mechanisms for transcriptional, posttran-scriptional, and translational control of expression, including alternative transcriptional initiation, read-through of termination signals, alternative splicing, and leaky ribosomal scanning. Although splicing is also found in Orthomyxoviridae (segmented, negativestrand RNA viruses), it is unprecedented in Mono-negavirales.

Virions are stable at 37°C and lose only minimal infectivity after 24 hr of incubation in the presence of serum. Virus infectivity is rapidly lost by heat treatment at 56°C and exposure to pH 5.0, organic solvents, detergents, chlorine, formaldehyde, or UV radiation.

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