HEMO 2025 / III Simpósio Brasileiro de Citometria de Fluxo
Mais dadosHIV infection affects over 40 million people globally. Antiretroviral therapy has transformed HIV into a chronic, manageable condition, with life expectancy now approaching that of the general population. As people living with HIV (PLHIV) age, hematological and non-hematological comorbidities requiring autologous stem cell transplantation (ASCT) are increasingly common. While ASCT is feasible in selected PLHIV, the impact of HIV on engraftment kinetics remains poorly defined, limiting evidence-based optimization of transplant strategies.
AimThis study evaluated the association of HIV infection with infusion-related adverse events and outcomes after ASCT.
Material and methodosIn this nested case-control study, 114 patients underwent ASCT at six Brazilian centers (2014–2025), with cryopreservation at a single facility. Nineteen (16.7%) were HIV-positive; all had positive serology at clinical/social screening and HPC collection, and four also had positive NAT results. Each case was matched by age, sex, diagnosis, and center to five HIV-negative controls. Data abstraction captured mobilization parameters, cell yield/viability, engraftment times, and infusion-related adverse events. Engraftment was defined as the time from infusion (Day 0) to neutrophil > 0.5 × 10⁹/L for three days, leukocyte > 1 × 10⁹/L for three days, or platelet >20 × 10⁹/L for seven days without transfusion.
ResultsBaseline characteristics were balanced between groups. Infusion-related adverse events were infrequent, with nausea, vomiting, flushing, and fever occurring in < 10% of participants, and rates were similar between HIV-positive (11.8%) and HIV-negative (16.3%) groups. Mobilization parameters, collection yield, and cell viability did not differ by HIV status. In unadjusted analyses, platelet engraftment occurred later in HIV-positive participants. Multivariable analysis confirmed HIV-positive status as an independent predictor of delayed platelet engraftment (β = 1.85 days; 95% CI: 0.63–3.07; p = 0.003) and leukocyte engraftment (β = 1.002 days; 95% CI: 0.13–1.87; p = 0.025). Neutrophil engraftment was not significantly associated with HIV status (p = 0.075). Higher infused CD34⁺ doses were consistently associated with faster recovery across all cell lineages, whereas the use of 10% DMSO as the cryopreservation solution was associated with longer engraftment times.
Discussion and conclusionIn conclusion, this study provides novel evidence that HIV infection independently delays platelet and leukocyte engraftment after ASCT, even when controlling for cell dose and other key transplant variables. The magnitude of the effect on platelet recovery is clinically meaningful, with potential to increase bleeding risk, prolong transfusion dependence, and delay full hematologic recovery. These findings underscore the need for tailored supportive care, optimized CD34⁺ collection, and proactive post-transplant monitoring in PLHIV. By addressing modifiable factors and integrating HIV-specific considerations into transplant planning, clinicians may mitigate the adverse impact of HIV on hematopoietic recovery. Future multicenter prospective studies with comprehensive immunologic profiling are warranted to elucidate underlying mechanisms and inform evidence-based guidelines. Overall, HIV infection should be recognized as an independent predictor of delayed engraftment after ASCT, reinforcing the importance of individualized transplant strategies for this population.




