A Pre-Transplant Humoral Immunity Score to Identify Risk of Severe Infection in Heart Recipients. A Multicenter Study

s S105 Purpose: We hypothesize that by individualizing antiviral prophylaxis according to their CMV immune response, and continuing valganciclovir until CMV-specific T-cell immunity has been established the incidence of late CMV reactivation will be reduced. We provide an interim analysis of 49/130 lung transplant (LTx) patients who have completed an interventional study of CMV-specific immune monitoring to direct the length of antiviral prophylaxis. Methods: LTx recipients were randomized 1:2 to either standard of care (cessation of antiviral prophylaxis at 5 months) or the need for continued antiviral prophylaxis as determined by the QuantiFERON-CMV assay. Those with a negative result received up to an additional 6 months of antiviral prophylaxis. The primary end-point of the study will be the incidence of CMV reactivation in the lung allograft within 18 months of LTx. Monthly blood monitoring for CMV was performed for 6 months after cessation of Valganciclovir. CMV reactivation within the lung allograft was assessed at bronchoscopy performed 9, 12 and 18 months after LTx. Results: An interim analysis of 49 LTx patients (female 57%, COPD 59%, mean age 56 years, Basiliximab 29%) was performed. CMV risk profiles defined by donor (D) and recipient CMV serostaus included D+/R+ (n = 20), D+/R(n = 12) and D-/R+ (n = 17). Low level late CMV reactivation (PCR u003e 150 copies) was common in both the blood (43%) and BAL (55%). Adopting a QFN-CMV directed approach to antiviral prophylaxis significantly reduced the incidence of severe viremia (40% vs 6%), with a less dramatic reduction seen in the lung allograft (33% vs 21%). The magnitude of the QFN-CMV response impacted on the subsequent risk of late severe CMV viremia, that was seen in 35% of LTx patients with a QFN-CMV response 1. Conclusion: A QFN-CMV directed approach significantly reduces late CMV viremia in LTx patients. Persistent CMV reactivation within the transplanted lung suggests that conventional CMV-specific T-cells may be less effective in the MHC-mismatched allograft.