Arch Virol (2000) 145: 127–147 Neuron-glia interactions in the rat retina infected by Borna disease virus J. Kacza 1 , T. W. Vahlenkamp 2 , H. Enbergs 2 , J. A. Richt 3 , A. Germer 4 , H. Kuhrt 4 , A. Reichenbach 4 , H. Müller 2 , C. Herden 3 , T. Stahl 1 , and J. Seeger 1 1 Institute of Veterinary Anatomy, Faculty of Veterinary Medicine, University of Leipzig, Leipzig, Germany 2 Institute of Virology, Faculty of Veterinary Medicine, University of Leipzig, Leipzig, Germany 3 Institute of Virology, Justus-Liebig University Giessen, Giessen, Germany 4 Paul-Flechsig-Institute for Brain Research, Department of Neurophysiology, Faculty of Medicine, University of Leipzig, Leipzig, Germany Accepted June 23, 1999 Summary. Neuron-glia interactions in the Borna disease virus (BDV)-infected rat retina were investigated with emphasis on the ultrastructural characterization of degenerative alterations in the ganglion cell and photoreceptor layer. Immuno- and cytochemical techniques were applied to label microglia, macrophages and Müller (macroglial) cells. Four weeks after intracerebral infection of adult rats, the total thickness of the retina was considerably diminished, primarily due to the loss of photoreceptor segments and ganglion cells. A gradual reduction of both plexiform layers was also observed. There was a remarkable increase in the number of microglial cells, predominantly in the ganglion cell and the in- ner plexiform layers. Ultrastructural analysis confirmed that microglia, but also macrophages, were involved in phagocytosis accompanying severe neuronal de- generation in the ganglion cell and the photoreceptor layer. In contrast, Müller cells showed moderate morphological and cytochemical alterations, indicating that Müller cells play only a minor role in early stages of BDV-induced retinitis. Monitoring neuron-glia interactions in BDV-induced retinopathy, combined with the application of different protocols of immunosuppression effecting the BDV virus and/or the microglia, might help to establish specific strategies to suppress BDV-induced neuronal degeneration. Introduction Animals infected with Borna disease virus (BDV) provide an important experimental model for the investigation of mechanisms involved in virus-induced