/94 virus, a parainfluenza type 1 virus recovered by lysolecithin fusion of multiple sclerosis brain cell cultures with CV-1 cells, replicated in monocyte macrophages and lymphocytes from normal human donors and from a patient with multiple sclerosis. In macrophage cultures, hemadsorption-positive cells and high levels of infectious virus became apparent within 24 to 48 h after infection, persisted for 6 days, and then began to decrease. Phytohemagglutinin-stimulated macrophages yielded similar titers of virus, but the levels were maintained for a longer period of time. Macrophage-produced virus appeared to be infectious for other macrophages in the same culture. Both unstimulated and phytohemagglutinin-stimulated lymphocytes also supported virus replication. Significantly higher titers were produced in the stimulated cultures, T cell-enriched populations producing more virus than unseparated populations whether stimulated or unstimulated. The presence or absence of antibodies to the virus in the donors did not appear to influence the levels of virus obtained in any of the leukocyte cultures. However, an increase in blastic forms after 6/94 virus infection was noted in lymphocytes from donors with antibodies as revealed morphologically and by increased incorporations of tritiated thymidine. Furthermore, 6/94 virusinfected lymphocytes, unlike Sendai virus-infected lymphocytes, were able to respond well to mitogenic stimulation by phytohemagglutinin. Two preceding papers (22, 23) described studies on the interaction of mouse macrophages and lymphocytes with 6/94 virus, an agent recovered from brain cell-derived cultures from two patients with multiple sclerosis (MS) after lysolecithin-mediated fusion with CV-1 cells (20). The results of these studies indicated that the virus replicated in both macrophages and unstimulated lymphocytes. Of interest was the finding that macrophages and lymphocytes derived from immunized mice that had high levels of specific humoral neutralizing antibodies were still variably susceptible to 6/94 infection. Zisman and Denman (26) reported that Sendai virus, an antigenic relative of the 6/94 agent (13), was inactivated by human and mouse lymphocytes independent of the presence of humoral antibodies. Differences in infectivity between 6/94 and Sendai viruses for mouse macrophages (4, 22) and lymphocytes (23, 26) made it of interest to investigate the interaction of 6/94 virus with human leukocytes.