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Borna virus replicated persistently in the brains of rats, causing frenzied and apathetic behavioral states in sequence but no mortality. The transient frenzied behavior was caused by an immune-mediated, cytolytic, encephalitic response that was unexpectedly self-limiting. Cessation of active pathological processes coincided with the onset of the passive phase of the disease. This study thus demonstrates suppression of virus-specific inflammation despite continuous viral replication and describes a new mechanism by which chronic encephalitis may become established.

Borna disease virus causes a rare meningoencephalitis in horses and sheep and has been shown to produce behavioral effects in some species. The possibility that the Borna virus is associated with mental disorders in humans was evaluated by examining serum samples from 979 psychiatric patients and 200 normal volunteers for the presence of Borna virus-specific antibodies. Antibodies were detected by the indirect immunofluorescence focus assay. Antibodies to the virus were demonstrated in 16 of the patients but none of the normal volunteers. The patients with the positive serum samples were characterized by having histories of affective disorders, particularly of a cyclic nature. Further studies are needed to define the possible involvement of Borna virus in human psychiatric disturbances.

Borna disease virus is an unclassified agent that causes a rare but fatal encephalitis in horses in Germany. In experimental animals the virus causes acute fatal encephalitis in some instances and chronic encephalitis with abnormal behavior in others. In initial studies of the pathogenesis of the latter disease in rats, the virus was shown to replicate only in the nervous system, with the greatest concentration of infectivity in the cerebrum and eyes. Viral replication continued indefinitely in both newborn and adult rats. The adult animals developed self-limiting, necrotizing encephalitis in the cerebrum, with inflammation spreading to the retina. Inflammation receded after two months, however, with concomitant cessation of necrosis; static hydrocephalus was observed at this point. Levels of viral replication were unaffected by these changes. Rats became frenzied and aggressive during the encephalitic period but became permanently passive and inactive after inflammation receded. Infected neonates and immunosuppressed adults did not become ill. The frenzied behavior and subsequent blindness in immunocompetent adults were therefore attributed to a uniquely transient immunopathologic reaction targeted to centers in the limbic system and retinal neurons.

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