Abstract
The neurotropic virus, Borna disease virus (BDV), a member of a group of nonsegmented, negative strand ribonucleic acid (RNA) viruses (order Mononegavirales), infects warm-blooded animal species. Infection among mammals may be asymptomatic, produce neurobehavioral abnormalities, or result in fatal meningoencephalitis. It is unique among animal viruses in the order Mononegavirales in its nuclear localization of replication and transcription and distinctive in its capacity to establish persistent, non-cytolytic infection of the peripheral and central nervous systems. Natural infection, long described in horses and sheep, has more recently been recognized to extend to bird species in association with a related virus, avian bornavirus, as well as to divergent bornaviruses in reptiles, challenging established virus taxonomy. Nonhuman primates can be experimentally infected; however, natural infection of humans and nonhuman primates appears to be unusual. Decades-long controversy over a role for BDV infection in human neuropsychiatric illnesses has more recently waned. Nonetheless, the discovery that the genomes of humans as well as other vertebrate lineages contain remnants of BDV sequences has raised questions regarding potential evolutionary implications. Analysis of rodent models of infection has yielded insights into the mechanisms by which neurotropic agents and host immune and signaling pathway responses may impact upon developing or mature CNS circuitry to effect complex neurobehavioral disturbances.
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Hornig, M. (2016). Borna Disease Virus. In: Reiss, C. (eds) Neurotropic Viral Infections. Springer, Cham. https://doi.org/10.1007/978-3-319-33133-1_13
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