Abstract
Infection with cytomegalovirus (CMV) remains a major problem in kidney transplant recipients, resulting in serious infectious complications and occasionally mortality. Accumulating evidence indicates that natural killer cell immunoglobulin-like receptors (KIRs) and their ligands affect the susceptibility to various diseases, including viral infections (e.g., CMV infection). We investigated whether KIR genes and their ligands affect the occurrence of CMV infection in a group of 138 kidney transplant recipients who were observed for 720 days posttransplantation. We typed the recipients for the presence of KIR genes (human leukocyte antigen C1 [HLA-C1], HLA-C2, HLA-A, HLA-B, and HLA-DR1) by polymerase chain reaction with sequence-specific primers. The multivariate analysis revealed that the lack of KIR2DS2 (p = 0.035), the presence of KIR2DL3 (p = 0.075), and the presence of KIR2DL2–HLA-C1 (p = 0.044) were risk factors for posttransplant CMV infection. We also found that a lower estimated glomerular filtration rate (p = 0.036), an earlier time of antiviral prophylaxis initiation (p = 0.025), lymphocytopenia (p = 0.012), and pretransplant serostatus (donor-positive/recipient-negative; p = 0.042) were independent risk factors for posttransplant CMV infection. In conclusion, our findings confirm that the KIR/HLA genotype plays a significant role in anti-CMV immunity and suggest the contribution of both environmental and genetic factors to the incidence of CMV infection after kidney transplantation.
Highlights
Despite the introduction of novel diagnostic and therapeutic modalities for the management of cytomegalovirus (CMV), it remains a significant cause of serious posttransplant complications, with high rates of mortality and graft loss [1]
Our results suggest that genotyping recipients for the KIR2DS2, KIR2DL2, and KIR2DL3 genes may help predict the occurrence of posttransplant CMV infection
The risk stratification for posttransplant CMV infection is primarily based on the assessment of donor and recipient (D/R) CMV serostatus prior to transplantation
Summary
Despite the introduction of novel diagnostic and therapeutic modalities for the management of cytomegalovirus (CMV), it remains a significant cause of serious posttransplant complications, with high rates of mortality and graft loss [1]. The immune response to CMV infection is complex The role of both adaptive and innate responses has not been well established in transplant recipients. Natural killer (NK) cells are effector cells that constitute a crucial part of the innate immune system and provide the first-line of defense against and control of CMV infection [6]. The inhibition and activation of the NK cell response is modulated by signals that include the interplay between polymorphic killer-cell immunoglobulin-like receptors (KIRs) and their ligands, human leukocyte antigen (HLA) class I molecules. The lack of ligands for inhibitory KIRs and the presence of activating KIRs in the recipient have been associated with a protective effect on the rate of CMV infection after kidney transplantation [11,12]
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