Murine AIDS (MAIDS) is a disease that shows many similarities with human AIDS. Several immunological parameters of the disease have been analyzed and genetic studies have mapped a gene (or genes) of resistance in the H-2 complex and shown that the genetic background of the mouse can significantly modify some features of the disease. The etiologic agent of MAIDS is a defective murine leukemia virus that seems able to induce disease in the absence of virus replication. This defective virus induces proliferation of its target cells and the cell expansion was found to be oligoclonal, thus suggesting that the immunodeficiency observed in these mice is a paraneoplastic syndrome. The excellent response of MAIDS mice to antineoplastic agents is consistent with this notion. This animal model has already been useful in stimulating the emergence of novel questions and the formulation of new hypotheses about human AIDS, namely about the role of defective HIV, the role of HIV replication in the progression of the disease, and the importance to identify the target cells of HIV in vivo. Although MAIDS and AIDS are not identical and are induced by retroviruses of different classes, the availability of such a model in an easily accessible small animal species, whose genetics is very sophisticated, may be instrumental in understanding the pathogenesis of AIDS if some of the cellular and molecular affected pathways are common in both diseases.