Bornavirus

An evolutionarily "old pathogen," Bornavirus is uncommonly genetically stable and contains highly conserved sequences. A member of the order Mononegavirales, it is most closely related to Paramyxoviridae and Rhabdoviridae. Although bornavirus has long been thought to be a classical animal virus, it has been shown to also be linked to human psychiatric disorders, including schizophrenia, paranoid psychosis and major depression. In animals, bornavirus is known to persist in the limbic system, a subarea of the central nervous system. The limbic system is known to affect mood, behavior, and memory. Hence, bornavirus was dubbed "sad horse disease" before it was known to have a large animal reservoir. Bornavirus is presently thought to be able to infect all mammals, including humans. As of yet, the virus has not been found in any other type of animals, such as birds, reptiles, or amphibians.

Neurons, where Borna persists

Pathogenesis

The clinical disease is still uncommon so that its pathophysiology is only partially understood. BDV is unusual in that it can exhibit lifelong persistence with short periods of activation and long periods of latency. For horses and sheep, its period of incubation is estimated to be approximately four weeks. The virus is thought to be spread by direct contact and exposure to the virus via saliva and nasal secretions. The olfactory route of transmission was proposed because intranasal infection is efficient and the olfactory bulbs of naturally infected horses show inflammation early in the disease. Experimentally, bornavirus can be induced by intracerebral injection or nasal innoculation. In experimentally infected animals, viral gene products are found in the saliva, urine and feces. Once in the body, bornavirus is capable of infecting all cell lines, but is primarily neurotropic. The agent enters the axons of peripheral nerves and spreads throughout the central nervous system. The way bornavirus effects the moods of its hosts is by targeting the limbic and hypothalamic regions. Although the exact neural mechanisms are unknown, bornavirus has been shown to cause changes in dopamine transmission. Although most bornavirus infections are subclinical, some infected horses and sheep are characterized by agitated aggressive behavior, which lasts for weeks, and progresses to paralysis and inanition. Although it is fatal in sheep and horses, borna disease virus is non-fatal in rats. Infected rats exhibit hyperactivity and exaggerated startle responses during the inflammation period. After several weeks, the virus persists and the animals begin to show stereotyped motor behavior, dyskinesias, and dystonias. After infection of the central nervous system, borna has been shown to progress to ganglia and the peripheral nerves.

Treatment and Prevention

Treatment for Borna is currently unknown although a recent study found that ribavirin inhibits borna replication, in the transcription step, at concentrations of 1-10 micrograms/ml in persistently infected cells. Conventional immunization with inactivated virus or purified virus-specific antigen does not provide immunity to clinical disease.

Structure and Morphology

Particles spherical, enveloped and 130 nm in diameter.

Spikes 7 nm in length.

Thin Nucleocapsid 4 nm in width.

Classification

Monopartite
Helical Capsid Morphology
Negative-stranded, single stranded 8.9 kbRNA
Enveloped
Spherical
Nuclear localization for replication and transcri ption
Posttranslational modification of subgenomic RNAs
Non-lytic
Non-cytopathogenic
Neurotropic

Computer-Generated Model of Bornavirus: