COINCIDENCE OF EPSTEIN-BARR-VIRUS REACTIVATION, CYTOMEGALOVIRUS-INFECTION, AND REJECTION EPISODES IN RENAL-TRANSPLANT RECIPIENTS

Reactivation of the Epstein-Barr virus was reported to occur frequentl y under immunosuppressive therapy following organ transplantation. How ever, little is known about the clinical significance of these EBV rea ctivations. Therefore, we searched for correlations among the treatmen t with various immunosuppressive drugs, the incidence of CMV infection s, rejection crises, and serological signs of EBV reactivation. EBV-sp ecific antibodies were measured with novel ELISAs, utilizing the recom binant antigens p72 (for anti-EBV nuclear antigen [EBNA]1-IgG), p54, a nd p138 (anti-early antigen [EA]-IgM, -IgG, -IgA) in a follow-up study of 79 renal transplant recipients, Patients receiving antithymocyte g lobulin or antilymphocyte globulin therapy showed increasing anti-EA-I gG and -IgA more often than did patients not receiving antithymocyte g lobulin or antilymphocyte globulin therapy (P < 0.05), In patients rec eiving OKT3 antirejection therapy, anti-EA-IgM seroconversion was foun d more frequently (P < 0.01). A significant correlation was also found between groups of patients who had had at least one rejection episode versus patients without any sign of organ rejection, and the incidenc e of increasing anti-EA-IgG: (P < 0,05). Since in most of these patien ts signs of EBV reactivation followed the appearance of the rejection episode, this may not be due to viral-induced rejection but may be cau sed by the reinforced immunosuppression during antirejection therapy. As opposed to patients with no signs of CMV infection and with nonsymp tomatic CMV infection, patients undergoing symptomatic CMV infection s howed anti-EA-IgM seroconversion (P < 0.01), increasing anti-EA-IgA (P < 0.01), and decreasing anti-EBNA-IgG (P < 0,01) more frequently, Our results confirm the role of immunosuppressive therapy in the pathogen esis of EBV reactivation. We further demonstrate a striking coincidenc e of EBV reactivation and symptomatic CMV infection.