Introduction: Human cytomegalovirus (HCMV) is an important pathogen after allogeneic bone marrow transplantation (allo-BMT). Post-transplant HCMV reactivation can lead to target organ damage and increased transplant-related mortality. However, HCMV reactivation has also been associated with a significantly reduced risk of leukaemia relapse after allo-BMT. The aim of this study is to investigate the effect that MCMV has on graft-versus-leukaemia (GvL) response and to identify the mechanism determining this effect. Materials and methods: Mice were infected with murine cytomegalovirus (MCMV) and following viraemia clearance, used as either donors or recipients in allo-BMT. Lethally irradiated recipient mice were transplanted with donor BM and T cells, and challenged with GFP+ primary murine myeloid leukaemia cells (derived by insertion of MLL-AF9 oncogene) on the day of transplant. Recipients were monitored for graft-versus-host diseases (GvHD), leukaemia burden and MCMV reactivation by clinical scoring, flow cytometry and qPCR, respectively. Two models of allo-BMT were used: MHCmismatched transplant using Balb/c (H-2Dd ) donors and C57Bl/6 (H-2Db ) recipients and MHChaploidentical transplant with C57Bl/6 (H-2Db ) donors and B6D2F1 (H-2Dbd) recipients. Results and Conclusions: Leukaemia survival was significantly improved in recipients of MCMVseropositive donors versus MCMV-seronegative donors in MHC-mismatched model (median survival: 41 vs 31 days, p < 0.05) but not in MHC-haploidentical allo-BMT. We demonstrated that the stronger GvL effect was independent of NK cells but was associated with distinct transcriptomic profiles in CD4 and CD8 T cells post-transplant, the validation of which is ongoing.