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EBV load, as measured by quantitative PCR in whole blood or plasma, mirrors clinical status in transplant recipients. Nearly every human becomes infected during childhood or adolescence, at which time the viral load climbs until the infection is brought under control by the immune system. Humoral and cell-mediated immunity established during primary infection helps maintain viral quiescence for the remainder of the person’s life, with latent EBV DNA retained for life in a small subset of B lymphocytes. Healthy carriers have measurable EBV DNA in whole blood, whereas plasma rarely contains EBV DNA at levels exceeding the lower limit of detection. When a transplant patient is iatrogenically immunosuppressed to prevent graft rejection, active viral infection results in higher baseline viral loads in both whole blood and plasma. Levels often rise before clinical diagnosis of posttransplant lymphoproliferation (PTLD), allowing preemptive intervention in high-risk patients who are routinely monitored for EBV levels. Successful intervention is marked by a return to baseline. A child or a rare adult who was never infected before onset of iatrogenic immunosuppression lacks prior immunity, placing the patient at high risk for active viral infection and progression to neoplasia. | Gulley, M. L., & Tang, W. (2010). Using Epstein-Barr Viral Load Assays To Diagnose, Monitor, and Prevent Posttransplant Lymphoproliferative Disorder. Clinical Microbiology Reviews, 23(2), 350 LP – 366. https://doi.org/10.1128/CMR.00006-09

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