Poster Session II: Acute myeloid leukemia - Biology - translational research
Cytomegalovirus (CMV) infection is a major cause of morbidity and mortality in hematopoietic stem cell transplantation (HSCT). Interestingly, in recent studies, CMV infections have been shown to have potential anti-leukemia effects in acute myeloid leukemia (AML) patients after HSCT. However, studies of CMV infection on relapse after single cord blood transplantation (CBT) are limited, and the effect of the virus load on relapse has not been assessed.
We hypothesize that the role of MCV on outcomes in CBT are related to virus load. In this study, we retrospectively analyzed the effect of CMV infection on two-year outcomes in 151 patients with AML after CBT according to the virus load. Additionally, the mechanism of the possible interaction with lymphocyte subsets was also analyzed.
We comparatively analyzed the outcomes of the high virus load group (CMV DNA copies ≥ 1 000/mL) and the low virus load group (CMV DNA copies <1 000/mL or negative CMV DNA copy) of two years after CBT. Furthermore, in order to explore the mechanism of CMV on relapse, a smaller cohort of 26 patients with immune reconstruction data at 1, 3, 6, 9 and 12 months after transplantation were simultaneously studied, and nine healthy physical examination populations were recruited as healthy controls.
The results showed that the high CMV virus load group had a lower two-year cumulative incidence of relapse (Figure A, 2.2% vs. 15.2%, p = 0.008) without an increase in non-relapse mortality (Figure B, 20.9% vs. 22.4%, p = 0.970) than the low CMV virus load group. Furthermore, the two groups had similar overall survivals (76.8% vs. 72.4%, p = 0.746). Moreover, the proportion and absolute number of CD8+ T cells were increased in the high CMV virus load group in different months after transplantation (Figure C and D).
In conclusion, a high CMV virus load in AML patients after CBT indicated a lower incidence of relapse, and this anti-leukemic effect might be mediated by the CMV-driven expansion of CD8+ T cells.