EBV Reactivation After Allogenic Hematopoietic Stem Cell Transplantation with PTCy-based GVHD Prophylaxis
Poster #: 079
Session/Time: B
Author:
William Christopher Glembocki, BS
Mentor:
Genovefa Papanicolaou, MD
Research Type: Clinical Research
Abstract
INTRODUCTION:
Epstein-Barr Virus (EBV) reactivation after hematopoietic stem cell transplantation (HCT) may lead to the development of Post-Transplant Lymphoproliferative Disease (PTLD), a potentially lethal condition. Post-Transplant Cyclophosphamide (PTCy), a form of selective T-cell depletion, is increasingly used for preventing Graft-Versus-Host Disease (GVHD) after HCT but has been associated with an increased risk for viral infections. We report Memorial Sloan Kettering Cancer Center's institutional experience with EBV reactivation in HCT with PTCy-based GVHD prophylaxis.
METHODS:
We conducted a retrospective cohort study of adult patients who received initial HCT from January 2017 to June 2024 with PTCy-based GVHD prophylaxis and were monitored routinely for EBV by quantitative polymerase chain reaction (qPCR). EBV reactivation severity was categorized as 1) viremia, 2) viremia requiring preemptive treatment with rituximab, and 3) viremia with probable or proven PTLD by PET scan or biopsy, respectively. We used R for statistical computing in evaluating cumulative incidence of EBV viremia, assessing the spectrum of reactivation, and univariate logistic regression analysis of factors relating to PTLD development.
RESULTS:
There were 412 patients in our study, and 65 of these patients developed EBV viremia within one year of HCT. We found the total cumulative incidence of EBV viremia after one year was 15.78%, with a 95% confidence interval of 12.25% - 19.30%. The spectrum of EBV reactivation was observed as follows: Out of 65 patients who developed EBV viremia, 18 received rituximab, 10 patients had probable PTLD, and 0 patients had proven PTLD. Univariate logistic regression analysis demonstrated Anti-Thymocyte Globulin (ATG) was a significant risk factor for both receiving rituximab treatment and probable PTLD (p < 0.01), with respective odds ratios of 8.56 and 18.7. Receiving a transplant from an unmatched or haploidentical donor versus a matched donor was a significant risk factor for developing EBV viremia (p < 0.01), with an odds ratio of 4.44.
CONCLUSION:
In our cohort of 412 HCT patients treated with PTCy, the total cumulative incidence of EBV viremia was 15.78%. 4.4% of all patients in the study received treatment with rituximab, and 2.4% developed probable PTLD. We found no cases in which PTLD was refractory to treatment with rituximab, nor were any deaths attributed to PTLD. Patients receiving ATG prophylaxis were more likely to receive rituximab treatment, and patients transplanted with an unmatched/haploidentical donor were more likely to develop EBV viremia. This single-institution study was limited by following patient outcomes for one year after HCT and by a lack of proven PTLD based on biopsy findings.
Epstein-Barr Virus (EBV) reactivation after hematopoietic stem cell transplantation (HCT) may lead to the development of Post-Transplant Lymphoproliferative Disease (PTLD), a potentially lethal condition. Post-Transplant Cyclophosphamide (PTCy), a form of selective T-cell depletion, is increasingly used for preventing Graft-Versus-Host Disease (GVHD) after HCT but has been associated with an increased risk for viral infections. We report Memorial Sloan Kettering Cancer Center's institutional experience with EBV reactivation in HCT with PTCy-based GVHD prophylaxis.
METHODS:
We conducted a retrospective cohort study of adult patients who received initial HCT from January 2017 to June 2024 with PTCy-based GVHD prophylaxis and were monitored routinely for EBV by quantitative polymerase chain reaction (qPCR). EBV reactivation severity was categorized as 1) viremia, 2) viremia requiring preemptive treatment with rituximab, and 3) viremia with probable or proven PTLD by PET scan or biopsy, respectively. We used R for statistical computing in evaluating cumulative incidence of EBV viremia, assessing the spectrum of reactivation, and univariate logistic regression analysis of factors relating to PTLD development.
RESULTS:
There were 412 patients in our study, and 65 of these patients developed EBV viremia within one year of HCT. We found the total cumulative incidence of EBV viremia after one year was 15.78%, with a 95% confidence interval of 12.25% - 19.30%. The spectrum of EBV reactivation was observed as follows: Out of 65 patients who developed EBV viremia, 18 received rituximab, 10 patients had probable PTLD, and 0 patients had proven PTLD. Univariate logistic regression analysis demonstrated Anti-Thymocyte Globulin (ATG) was a significant risk factor for both receiving rituximab treatment and probable PTLD (p < 0.01), with respective odds ratios of 8.56 and 18.7. Receiving a transplant from an unmatched or haploidentical donor versus a matched donor was a significant risk factor for developing EBV viremia (p < 0.01), with an odds ratio of 4.44.
CONCLUSION:
In our cohort of 412 HCT patients treated with PTCy, the total cumulative incidence of EBV viremia was 15.78%. 4.4% of all patients in the study received treatment with rituximab, and 2.4% developed probable PTLD. We found no cases in which PTLD was refractory to treatment with rituximab, nor were any deaths attributed to PTLD. Patients receiving ATG prophylaxis were more likely to receive rituximab treatment, and patients transplanted with an unmatched/haploidentical donor were more likely to develop EBV viremia. This single-institution study was limited by following patient outcomes for one year after HCT and by a lack of proven PTLD based on biopsy findings.