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Quantification of BKV-load and BKV-specific immunity have been evaluated to monitor BKV-replication and outcomes in kidney transplant recipients (KTRs) with BKV-infection. However, it remains crucial to better understand how immune markers can predict the risk for later infection. We studied all KTRs between 2008 and 2011. Twenty-four KTRs were diagnosed with BKV-replication and a control group of 127 KTRs was used for comparison. Samples were collected before at +1, +2, and +3 months posttransplantation. BKV-specific and alloreactive T cells were measured using an interferon-γ Elispot assay. The extent of immunosuppression was quantified by lymphocyte subpopulations and interferon-gamma levels. KTRs with a loss of BKV-specific T cells directed to Large T-antigen from pretransplantation to posttransplantation were at increased risk of BKV-replication (p < 0.001). In contrast, KTRs with stable/rising BKV-specific T cells were more likely not to develop BKV-replication (p < 0.05). KTRs developing BKV-replication showed significantly lower CD3+, CD4+, CD8+ T cells and interferon-γ levels posttransplantation, but significantly higher alloreactive T cells (p < 0.05). Monitoring pretransplant and posttransplant BKV-specific T cells is suggested a sensitive marker to identify KTRs at increased risk of BKV-replication. Increased susceptibility to immunosuppression predisposes KTRs to a loss of protective BKV-specific immunity that results in impaired virus control and BKV-replication.
© Copyright 2015 The American Society of Transplantation and the American Society of Transplant Surgeons.
T cell biology; alloantigen; basic (laboratory) research / science; clinical research / practice; immunosuppression / immune modulation; infection and infectious agents; infectious disease; kidney transplantation / nephrology; viral: BK / JC / polyoma; viral: Cytomegalovirus (CMV)