Mice homozygous for the autosomal recessive mutation severe combined immune deficiency (scid) on Chromosome 16 have proved to be a unique resource in many areas of biomedical research. Since the original report that hdmozygosity for scid causes a severe deficiency in numbers of functional T and B cells accompanied by a lack of both humoral and cell-mediated immune function (Bosma et al.1983), numerous investigations have focused on the molecular basis of defective immunoglobulin and T cell receptor production and on the selective nature of the lymphocyte depletion in these mice (Shultz and Sidman, 1987). In addition to the value of the acid mutation as a tool to increase our understanding of the molecular events underlying lymphocyte development, recent reports have described the use of scid/scid mice as models to study development of human lymphoid cells following transplantation of human fetal tissues (McCune et aI. 1988) and to study interactions occuring during the course of infection of human cells with human immunodeficiency virus (HIV) (Namikawa et al. 1988).