Borna disease, a naturally occurring encephalomyelitis of horses and sheep, was induced in rhesus monkeys after intracerebral infection with virus containing rabbit brain suspension. The animals developed neurological disorders followed by a severe encephalomyelitis which was accompanied by a retinopathy. In all the analyzed brain and retina tissue pieces, virus-specific antigen could be demonstrated by immunoelectrophoretic techniques. Antibodies could be demonstrated by the intermediate gel technique as well as by the immunofluorescence test in the serum and the cerebrospinal fluid of all the monkeys. The histopathological findings in the brain and the eye might be comparable to certain types of encephalitis in man and to pathological changes in the eye of human patients, the etiologies of which are still obscure. An attempt was also made to study cell-mediated immunity by a chromium release assay in infected animals, the results of which might provide, together with the histopathological observations, strong evidence for the role of lymphocytes in the pathogenesis of BD infection in rhesus monkeys.

Selective damage of the optic nerve of 14 rabbits without interfering with the choroidal blood flow which supplies the retina and without altering the autonomic nerve supply was successfully achieved by Xenon coagulation. This procedure interrupted the axonal pathway between the brain and the eye. After experimental infection with Borna disease virus the typical disease could be induced. The pathognomonic retinopathy as well as characteristic perivascular choroidal infiltrates, however, did not appear in eyes with coagulated nerve heads. In general virus-specific antigen or infectious virus were not present in the retinas of such damaged eyes. These results permit the conclusion that the ocular expression of Borna disease is a consequence of virus transport via the optic nerve.

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