Dr. Harter has given a very good, complete description of the general properties of visna virus, referring briefly to the disease process and the problems of pathogenesis. Some of the work on the pathogenesis of Visna currently being carried out at our institute in collaboration with G. Georgsson, P. A. Pálsson, H. Panitch, and N. Nathanson defines the role of immunologic responses of visna-infected sheep in the pathogenesis of the disease. In the early days of these investigations, M. Gudnadóttir and P. A. Pálsson infected a group of 24 sheep with visna virus and reported that the preclinical incubation period varied from 3 months to 8.5 years. Two of the animals were killed close to the end of their normal lifespan without ever developing signs of the disease. The infection is slow indeed. If animals are studied during this silent incubation period, however, the development of pathologic changes is not seen to be very slow after all. As early as 2 weeks after intracerebral injection, some animals display pleocytosis of the cerebrospinal fluid (CSF). In most animals, this reaches a maximum 1 month later and then slowly decreases in an irregular manner. The majority of the sheep continued to have elevated CSF cell counts during the first year of infection.