The maedi-visna virus (MVV) is classified as a lentivirus of the retroviridae family. The genome of MVV includes three genes: gag, which encodes for group-specific antigens; pol, which encodes for reverse transcriptase, integrase, RNAse H, protease and dUTPase and env, the gene encoding for the surface glycoprotein responsible for receptor binding and entry of the virus into its host cell. In addition, analogous to other lentiviruses, the genome contains genes for regulatory proteins, i.e. vif, rev and tat. The coding regions of the genome are flanked by long terminal repeats (LTR) which play a crucial role in the replication of the viral genome and provide binding sites for cellular transcription factors. The organs targeted by MVV are, in descending order of importance, the lungs, mammary glands, joints and the brain. In these organs, the virus replicates in mature macrophages and induces slowly progressing inflammatory lesions containing B and T lymphocytes. The clinical signs of MVV infection, i.e. dyspnea, loss of weight, mastitis and arthritis, are related to the location of these lesions. Infection with MVV induces the formation of antibodies which can be detected by agar gel immunodiffusion, ELISA and the serum neutralization assay. As neither antiviral treatment nor vaccination is available, diagnostic tests are the backbone of most of the schemes implemented to prevent the spread of MVV. However, since current serological assays are still lacking in sensitivity and specificity, molecular biological methods are being developed permitting the detection of virus in peripheral blood, milk and tissue samples. Future research will have to focus on both the development of new diagnostic tests and a better understanding of the pathogenesis of MVV infection.