Borna disease

Borna diseases viruses 1 and 2 appear to have wide host ranges, having been detected in horses, cattle, sheep, new world camelids, dogs, cats, and foxes.[7][8] In 1995, BoDV-1 was isolated from cats with a "staggering disease" in Sweden.[9] BoDV-1 has been detected in animals in Europe, Asia, Africa and North America.

Symptoms of Borna disease in horses and sheep start after a four-week incubation period followed by the development of immune-mediated meningitis and encephalomyelitis. Clinical manifestations vary but may include excited or depressed behaviour, ataxia, teeth grinding, excessive salivating, ocular disorders and abnormal posture and movement. Later stages are characterised by bouts of fever and flailing of limbs while lying down. Death occurs a few days to weeks after symptom onset. Mortality rates are 80-100% in horses and greater than 50% in sheep.

Experimental infection of rats has been demonstrated to lead to learning impairments and altered social behaviour. The virus appears to be distributed primarily in the limbic system of the brain, including the hippocampus and entorhinal cortex. These areas of the brain are considered to be of importance in emotion.

Avian bornaviruses, a group of related viruses, have been reported, yet not proven, as the cause of proventricular dilatation disease (PDD), a disease of pet parrots. The use of a 'positive' brain cell culture containing ABV to inoculate another psittacine (parrot) bird resulted in the inoculated bird's death and subsequent histopathological diagnosis of PDD (mononuclear infiltrative ganglioneuritis). Earlier research with purified avian bornavirus inoculant (while did result in the death of parrots) did not reproduce histopathological changes associated with PDD.

In 2018, three fatal cases of Borna disease in humans were confirmed in Germany.[10][11] Three people were suspected to have been infected via organ transplants from the same donor, two of whom died. A third fatal case was unconnected to the organ donation. All three deaths were due to severe encephalitis.[10][11]

In 2020, several additional cases of human infection were identified in the German federal state of Bavaria.[12] In total, there have been 24 cases of confirmed BoDV-1 infection of humans between 1996 and 2021 . The infection was almost always fatal. All cases occurred in known areas of spread of BoDV-1, including the federal states of Bavaria, Brandenburg, Thuringia, and Saxony-Anhalt.[3][13][14][15][16][17][18][19][20][21][22]

There is some evidence that there may be a relationship between BoDV-1 infection and psychiatric disease.[4][23]

In 1990, Janice E. Clements and colleagues reported in the journal Science that antibodies to a protein encoded by the BoDV-1 genome are found in the blood of patients with behavioral disorders.[24] In the early 1990s, researchers in Germany, America, and Japan conducted an investigation of 5000 patients with psychiatric disorders and 1000 controls, in which a significantly higher percentage of patients than controls were positive for BoDV-1 antibodies.[24] Subsequent studies have also presented evidence for an association between BoDV-1 and human psychiatric disorders.[25][26][27] However, not all researchers consider the link between BoDV-1 and human psychiatric disease to be conclusively proven. A study published in 2003 found no BoDV-1 antibodies in 62 patients with the deficit form of schizophrenia.[28]

Additional evidence for a role of BoDV-1 in psychiatric disorders comes from reports that the drug amantadine, which is used to treat influenza infections, has had some success in treating depression and clearing BoDV-1 infection.[29][30]