Borna disease virus is the virus that causes Borna disease.
It has the smallest genome (8.9 kilobases) of any Mononegavirales species and is unique within that order in its ability to replicate within the host cell nucleus.
Borna virus was isolated from a diseased horse in the 1970s, but the virus particles were difficult to characterise. Nonetheless, the virus' genome has been characterised. It is a linear negative-sense single stranded RNA virus in the order of the mononegavirales. This order contains the family of lyssaviruses which includes the viruses responsible for rabies. A new family named the bornaviridae was created to hold this virus.
Several of the proteins encoded by the Borna virus genome have been characterised. The G glycoprotein is important for viral entry into the host cell.
It has been suggested that the p10, or X, protein plays a role in viral RNA synthesis or ribonucleoprotein transport.
The P40 nucleoprotein from BDV is multi-helical in structure and can be divided into two subdomains, each of which has an alpha-bundle topology. The nucleoprotein assembles into a planar homotetramer, with the RNA genome either wrapping around the outside of the tetramer or possibly fitting within the charged central channel of the tetramer .
P24 (phosphoprotein 24) is an essential component of the RNA polymerase transcription and replication complex. P24 is encoded by open reading frame II (ORF-II) and undergoes high rates of mutation in humans. It [binds amphoterin-HMGB1, a multifunctional protein, directly and may cause deleterious effects in cellular functions by interference with HMGB1. Horse and human P24 have no species-specific amino acid residues, suggesting that the two viruses are related. Numerous interactions of the immune system with the central nervous system have been described. Mood and psychotic disorders, such as severe depression and schizophrenia, are both heterogeneous disorders regarding clinical symptomatology, the acuity of symptoms, the clinical course and the treatment response. BDV p24 RNA has been detected in the peripheral blood mononuclear cells (PBMCs) of psychiatric patients with such conditions. Some studies find a significant difference in the prevalence of BDV p24 RNA in patients with mood disorders and schizophrenia, whilst others find no difference between patients and control groups. Consequently, debate about the role of BDV in psychiatric diseases remains alive.
Bornaviruses enter the host by endocytosis. After this virus has entered its host it is taken up by endosomes. Replication of the bornavirus occurs inside the nucleus. This is the only animal virus within the order Mononegavirales to do this. Many plant Rhabdoviruses replicate in the nucleus.
Bornaviruses have negative sense RNA genomes  The negative sense RNA is copied to make a positive sense RNA template. This template is then used to synthesise many copies of the negative sense RNA genome. This is like making copies of a mold, and then using these molds to make many more viruses.
Endogenous provirus 
Endogenous viral elements homologous to the nucleoprotein gene of the Bornavirus have been shown to exist in the genomes of several mammalian species.
The Borna disease was first described in 1885 as "heated head disease" of cavalry horses in 1885 in the town of Borna, Germany.
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