Persistence of Sindbis virus (SV) was studied for 9 months in two lines of mouse cell cultures (BALB/C) in one of which the genome of endogenous ecotropic oncornaviruses was repressed. The other lines was exogenously infected at the level of plimary culture with Rauscher leukemia virus (RLV) and SV and showed gradual inhibition of oncornavirus functions. The presence of oncornavirus type C was not the necessary condition for the development of persistent SV infection, however it influenced the character of persistence. In both systems, sequential loss of the hemagglutinating and interferon-inducing activities, then infectivity of SV (61--82 days), and persistence of the noninfectious antigen of the arbovirus for 9 months were observed. The differences consisted in the time of appearance of homologous interference to SV: in the presence of oncornavirus earlier (40 days), under conditions of repressed oncornavirus genome later (179 days). Electron microscopic examinations showed that in the system infected with RLV and SV there occurred in the course of persistence a sharp activation of phagosome-lysosome complex accompanied by incorporation into phagocytolysomes of numerous intact and partially destroyed virions of SV and RLV and their release from cell with cytoplasmic fragments. Possible mechanisms of inhibition of functions of the oncogenic and infectious viruses in the reported model of mixed chronic infection are discussed.