Guinea-pig line 10 tumor (GPL10) cells, which were transplantable in strain 2 guinea-pigs, gained the capacity to activate the homologous alternative complement pathway (ACP) following infection with ultraviolet-irradiated Sendai virus (UV-SV). The ACP activation of homologous serum on the UV-SV-infected GPL10 cells (UV-SV-GPL10 cells) resulted in cytolysis of the tumor cells. This indicates that UV-SV infection induced not only the capacity to activate complement on the GPL10 cells, but also made them sensitive to complement attack, because GPL10 cells have been demonstrated to be resistant to the reaction of homologous complement via the classical pathway in the presence of rabbit antibody. Furthermore, UV-SV-GPL10 cells prepared with as little as 0.1 plaque-forming unit equivalent of UV-SV per cell showed suppressed growth in syngeneic strain 2 guinea-pigs. The essential role of complement in the elimination of UV-SV-GPL10 cells in vivo was confirmed by demonstrating that UV-SV-GPL10 could grow in guinea-pigs whose complement had been depleted by administration of cobra venom factor.