A type C RNA virus has been detected in the culture fluids of the SU-DHL-1 human histiocytic lymphoma cell line previously established in this laboratory. In electron micrographs, the virus closely resembled other typical mammalian type C RNA tumor viruses in size and morphology. Viral RNA-dependent DNA polymerase activity has been demonstrated in particles (densities of 1.15 and 1.22 g/ml) in the microsomal cytoplasmic fraction and in pellets of culture fluids. The enzyme is partially inhibited by antibodies to the RNAdependent DNA polyerases of simian sarcoma virus and RD-i 14 virus but not by antibody to the polymerase of murine leukemia virus, suggesting some degree of relatedness to type C viruses of subhuman primate origin. Typical syncytial microplaques were induced when SU-DHL-1 cells were cocultivated with rat XC cells. Although no focus formation was noted in similarly cocultivated mouse UC1-B cell cultures, the numbers of foci induced in rat embryo fibroblasts by murine sarcoma virus were significantly increased by coinfection with the virus from SU-DHL-1 cell culture fluids. No other evidence of infectivity, inducibility, or capacity for helper rescue of defective murine sarcoma virus genomes has been detected to date in cocultivation studies with a spectrum of fibroblastic and other nonlymphoid indicator cell lines of human and other species of origin. Type C RNA viruses have been identified as causative agents of leukemias, lymphomas, and sarcomas in avian, murine, feline, cavian, bovine, and subhuman primate species (cf. ref.