Importance of simultaneous active cytomegalovirus and Epstein-Barr virus infection in renal transplantation
1996; Elsevier BV; Volume: 6; Issue: 2-3 Linguagem: Inglês
10.1016/0928-0197(96)00230-9
ISSN1873-4901
AutoresThomas Meyer, D Scholz, G. Warnecke, Meik Kunz, R. Arndt, Udo Reischl, Hans Wolf, R. Lissner,
Tópico(s)Parvovirus B19 Infection Studies
ResumoAlthough being the most common infective complication after transplantation, cytomegalovirus (CMV) infection does not always produce disease symptoms in immunosuppressed patients. Development of CMV disease may depend on different factors such as virulence of particular CMV strains and impairment of CMV-specific immune reactions.Demonstration of the importance of simultaneous Epstein-Barr virus (EBV) activation for development of symptomatic CMV infections.208 renal transplantation patients were monitored for 3 years with respect to (i) CMV and EBV replications, and (ii) clinical symptoms associated with combined and single infections, respectively.CMV and EBV replications were observed in 22% and 19% of the patients, respectively. Many of these active virus infections were found to overlap in time (59% and 74% of all active CMV and EBV infections, respectively). The increased detection of combined CMV and EBV infections probably does not result from higher initial immunosuppression in these patients, since the percentage of patients receiving OKT3 or ATG was almost identical in the groups of single and combined infections. In 18 cases of combined infections, CMV replication preceeded EBV replication, while EBV replication prior to CMV replication was observed in one case only, indicating that activation of latent EBV infection may be induced during active CMV infection.Simultaneous replication of both viruses seems to be clinically important, since severe clinical symptoms were observed only in the group of combined CMV and EBV infections. Symptoms were similar to the clinical pictures of CMV disease. Thus, simultaneous EBV replication may be an important co-factor for the development of CMV disease, possibly by further decreasing the number of functional CD4 T cells or enhancing the CD8-positive cytolytic/suppressor T-cell subset as reflected by the comparatively stronger decrease of CD4/CD8 ratio during simultaneous CMV and EBV replication, particularly in the case of symptomatic infections.
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