Borna Disease was first described towards the end of 18th century in horses. The disease was recognized in central Europe as a spontaneous encephalopathy in horses and sheep by the late 1800s. Borna Disease virus (BDV) was discovered to be the cause of Borna disease, more than a century later, in 1926. Recent studies have not only detected BDV in humans, but have linked BDV with human neuropsychiatric disorders. This compelling link has spawned an extremely exciting and active area of research with bornaviruses.
Bornavirus is named after the city of Borna, located in Sauxony, Germany, where the disease made a continuous appearance between 1894 and 1896.
Natural hosts: Horses, sheep, cats, rabbits, humans
Sporadic infection in: dogs, donkeys, mules, ostriches, alpacas, pygmy hippopotami.
Experimental host range: Extremely wide, from birds to rodents to nonhuman primates
Natural Reservoir: Unknown, possible ticks?, possible rats?
In animals, onset of symptoms is variable, but is around 30 to 40 days after infection. There is no data regarding the incubation period in humans.
The method of transmission of the virus is unclear, especially in humans. Experimental data suggests transmission through exposure to virions in saliva, nasal and conjunctival secretions, blood, urine, or feces. This may be through contaminated food or water, or through direct contact. Recent studies show that an intranasal route of entry may be ideal for bornaviruses.
The virus is seasonal, and is more active during spring and early summer. BDV has an esxtremely wide host range, and can be found in Europe North America, Africa, and Asia. Clinical cases of BD in animals seem to be isolated to central Europe.
In humans, there is a higher BDV seroprevalence in neuropsychiatric patients, as well as the immunodeficient. These results have had a wide range, however, and there is poor information regarding its overall prevalence in humans. More research is necessary to clarify the relationship between BDV and humans.
In animals, initial clinical signs include movement abnormalities, aggressive behavior, excitability and hyperactivity. This is followed by a chronic phase of disease, characterized by apathy, somnolence, depression, and obesity.
Motality rates are extremely high in animals, ranging from 80 to 100% in horses, and 50% in sheep. Survivors are chronically infected and face recurring disease.
In rats, BDV infection in neonatal rats leads to an asymptomatic chronic infection. The rats do not show any symptoms, but they do show deficiencies in emotional function, cognitive ability, reduced body weight and length, impaired growth, and neurodevelopmental abilities.
Clinical symptoms, however, do not appear in all animals and may be species specific.
In animals, live-virus vaccines were used to protect sheep and horses, but have been discontinued as the live vaccines often transmitted infectious disease. Experimental evidence indicates the possibility of using passive immunization with BDV-specific CD4+ T cells or an attenuated BDV virus for preexposure prophylaxis in animals.
There is very little research done on treatment in humans. A recent, fairly exciting study showed that amatadine sulfate, an antiviral drug, could be used to inhibit BDV replication both in vitro and in vivo. Interestingly enough, usage of the antiviral drug was found to diminish depressive symptoms in patients with acute major depression or bipolar disorder depression. Ribavirin may also be a potential antiviral used to treat BDV.