Virus infection, as a rule, is associated with the development of cytopathic changes in the host cell both in vivo and in vitro. The study of persistent virus infections, however, has led to the recognition that this cytopathic change may evolve slowly and may even be minimal. At the end of the 1970s it became evident that some viruses may alter cell function even without causing any kind of morphological damage to the host cell (Oldstone 1984). During this process some of the differentiated functions of the cell suffered, while the vital functions could remain intact, securing survival of the cell. This phenomenon was first noted in vitro in murine neuroblastoma cell lines exhibiting a disturbance of acetylcholine (ACh) metabolism when persistently infected with lymphocytic choriomeningitis virus (LCMV) (Oldstone et al. 1977). In vivo infection of mice induced disturbance in growth hormone (GH) production and glucose metabolism; however, there were no lytic changes in the GH-producing somatotrophic pituitary cells, although replication of LCMV was restricted to this cell type of the anterior pituitary (Oldstone et al. 1982, 1984; Rodriguez et al. 1983). Another interesting observation emerged from experimental infection of mice with canine distemper virus, which induced severe obesity and other hormonal abnormalities. Cell destruction, however, could not be observed (Lyons et al. 1982).