Approximately 83% of the world’s population is seropositive for human cytomegalovirus (HCMV) and will endure lifelong latency. An immunocompromising disease such as HIV/AIDS increases susceptibility to reactivation and HCMV diseases. If an AIDS patient’s CD4+ T cell count falls below 50 cells/μL of peripheral blood, HCMV is reactivated which causes a sight-threatening retinitis. The disease affects up to 42% of AIDS patients and causes retinal necrosis. To further investigate the mechanisms of AIDS-related HCMV retinitis we studied RIPK3 stimulation in HCMV-infected ARPE-19 cells under oxidative stress, through pursuit of two experimental hypotheses: (1) HCMV-infected ARPE-19 cells will upregulate RIPK3 in the presence of oxidative stress induced by H2O2 and (2) HCMV-infected MRC-5 cells will not express RIPK3 stimulation in the presence of oxidative stress induced by H2O2. Our data suggests that RIPK3 stimulation presents a cell-specific dose-dependent response to H2O2 concentrations in ARPE-19 cells during HCMV infection.