The purpose of the experiments reported in this dissertation was to determine whether bovine immunodeficiency-like virus (BIV) is able to affect monocyte function in vivo or in vitro. Monocyte function assays included the phagocytosis of opsonized Staphylococcus aureus, antibody-dependent cell-mediated cytotoxicity (ADCC), and random and chemotactic migration. Initial experiments determined that monocyte function was relatively unchanged in a group of R29 BIV-infected cattle for the first 2.5 years post-inoculation. One BIV-infected calf developed a fatal atypical T cell lymphosarcoma, with a concurrent monocytosis. Monocyte function in this animal remained normal; however, virus was isolated from cultured monocytes of this animal much earlier (7 months PI) than from the other BIV infected animals in this experiment (18 months PI). Although BIV did not significantly affect monocyte function in experimentally infected animals, treatment of normal bovine monocytes with BIV-containing cell supernatants significantly (P < 0.05) decreased ADCC and increased phagocytosis, random migration and chemotactic migration, in a dose-dependent manner. Supernatants from BIV-infected cells contained 10-30 kD and 30-50 kD proteins which significantly (P < 0.05) increased monocyte chemotaxis. Affinity purification with monoclonal anti-p26 antibodies yielded preparations which were active in the random migration, chemotaxis, and phagocytosis assays, but did not affect ADCC. The activity of the affinity purified preparation could be specifically neutralized by hyperimmune rabbit serum against the BIV Gag proteins. A recombinant Gag protein, consisting mainly of BIV p26, also enhanced monocyte random and chemotactic migration. We have, therefore, found that direct treatment with affinity purified BIV Gag proteins, or with a recombinant Gag protein, is able to significantly affect the function of normal monocytes in vitro. The evidence indicates that the factors affecting monocyte migration and phagocytosis in vitro are one or more breakdown products of the BIV Gag precursor, particularly those containing the p26 capsid protein. Based on these results, it is possible that BIV infection in vivo alters monocyte function locally, at sites of virus replication.