Abstract: Boma Disease virus grows without any cytopathic effect in many cell lines (including those from man). It comprises an enveloped RNA-containing virion of ca. 100 nm. The infection induces major specific antigens known as p40 and p24.. Under natural conditions and in experimentally infected animals antibodies are produced against these antigens and determinants involved in neutralization of the virus. In the central nervous system (CNS) a local immune response accompanied by the production of oligoclonal immunoglobulins is demonstrable. Histopathologically, Boma disease often goes along with a non-purulent inflammation of the brain and the spinal cord. Most alterations are fOLind In the grey matter, mainly in the Ammon`s horn, olfactory lobe, caudate nucleus, thalamus, lamina quadrigemina and in the cerebellar nuclei. The perivascular infiltrations, consisting of lymphocytes, histiocytes and plasma cells are most conspicuous. Some animal species show typical intranuclear inclusion bodies (Joest-Degen inclusions) , which are composed of specific antigen and are located in ganglion cells of the Ammon`s hom, the piriform lobe and the retina. The portal of virus entry under natural conditions seems to be the olfactory bulb besides a vertical transmission of virus from mother to offspring. Experimentally, the infection is possible via different routes, but the age of the animal is also decisive. Virus spread occurs mainly intraaxonally. The diagnosis of Boma disease is established intra vitam on the basis of the clinical symptoms and the presence of antibodies in serum or cerebrospinal fluid (CSF), as well as by new ELISA methods measuring specific antigen and immune complexes. Post mortem the demonstration of specific antigen in the brain allows a definite diagnosis. It is more difficult to disclose infections by growing the virus in tissue culture and by animal inoculation. For the latter technique the 1 day old rat proved to be the most sensitive test system. Besides its significance for the practitioner, Boma disease virus infection remains to be unique as a disease model: it allows to study most diverse alterations in neurobiological processes. The great adaptability of the virus to different animal species and its affinity for neurons allow to investigate clinical alterations involving the CNS and to quantitate the virological and immunological interactions of the agent with nerve cells in the brain and the eye. The ability of Boma disease virus to cause persistent infections of neurons most probably plays the key role in pathogenetic events.