Several aspects of the interaction of macrophages and maedi visna virus (MVV) were undertaken: viral replication, phenotype, phagocytosis and antigen presenting function of macrophages after MVV (EV1) infection. MVV replication in monocyte-derived-macrophages (MDM) showed viral budding sites both at cytoplasmic and vesicular membranes. In contrast, viral budding sites predominantly occurred at the cytoplasmic membrane of skin fibroblasts, whilst vims accumulated in vesicular lumens of MVV-infected alveolar macrophages (AM). Many intracytoplasmic type A (ICA) particles accumulated in the cytoplasm of MDM and AM infected with EV1. Expression of MHC class II, MHC class I, CD4, CD8, LFA-1 and VPM32 antigen on MDM infected in vitro was unaltered by 5 days after MVV infection (P>0.05). In vivo MHC class I, class II (DQ & DR) and LFA-1 expression on AM from MVV infected sheep with lung lesions was greatly increased compared to uninfected sheep (P<0.05). A significant decrease in the CD4 : CD8 ratio in bronchoalveolar lymphocytes was also found in the same group. The phagocytic activity of macrophages after MVV infection was also studied both in vivo and in vitro. There was a decrease in the phagocytic activity for RBC (P<0.05) and yeast by MVV-infected MDM after 5 days post infection, but the FcR expression of MDM assayed by erythrocyte rosetting (ER) did not show a significant difference between MVV and mock infected MDM. In vivo, there was no significant difference in ER, phagocytosis of RBC and P. hemolytica by monocytes between MVV-infected and control sheep. However surface binding and phagocytosis of opsonized P. hemolytica by AM from MVV infected sheep without lung lesions was significantly increased compared to uninfected sheep (P<0.05), but this increase was not seen in ER and phagocytosis of RBC by AM in the same group. In contrast the ER, phagocytosis of RBC and P. hemolytica by AM from sheep with lung lesions was slightly lower, but not significantly different from uninfected sheep. A defect in antigen presenting function of MDM in vitro was also found 3-5 days after MVV infection by using ovalbumin and PPD specific T cell lines as responding cells. MVV-specific cytotoxic lymphocytes were activated by autologous MVV-infected skin fibroblasts, AM and MDM. MVV-infected MDM, AM and skin fibroblasts could be specifically lysed by MHC-specific and CD8+ cytotoxic lymphocytes (CTL). In addition, macrophages either infected or non-infected were non-specifically lysed by lymphokineactivated killer cells.