Abstract

Viruses are the main cause of opportunistic infections after kidney transplantation. The aim of this study was to determine the prevalence of cytomegalovirus (CMV), Epstein-Barr virus (EBV), B. K. virus (BKV) and John Cunningham virus (JCV) infections in renal transplant recipients (RTR). This retrospective study of 112 RTR investigated the presence of CMV, EBV and polyomaviruses DNA in plasma and/or urine by PCR. The visualization of PCR products was performed by electrophoresis on 2% agarose gel stained with ethidium bromide and photographed under a UV light. The chi-square test was used for statistical analysis. CMV DNA was detected in 14/112 (12.5%), EBV DNA in 4/49 (8.16%), BKV DNA in 10/31 (32.26%) and JCV DNA in 3/31 (9.68%) RTR. These results show that CMV infection is more often present in RTR compared to other investigated viral infections. In the light of these results, molecular testing could be useful in identifying recipients at high risk of symptomatic post-transplant viral infection.

Highlights

  • The human body has a complex system of protective mechanisms to prevent infection which involves both adaptive and innate immune systems

  • All 112 patients were monitored for CMV DNA, 49 for Epstein-Barr virus (EBV) DNA in plasma samples, and 31 transplant recipients were investigated for B. K. virus (BKV) and John Cunningham virus (JCV) DNA in plasma samples and urine using a PCRbased test

  • Forty-nine blood samples from pediatric patients were tested for the presence of EBV DNA by PCR and only 4/49 (8.16%) samples were positive (Table 3)

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Summary

Introduction

The human body has a complex system of protective mechanisms to prevent infection which involves both adaptive and innate immune systems (e.g. skin, mucus membranes). Solid organ and bone marrow transplantation are among the most important advances in modern medicine Their success depends to a great degree on the ability to control and manage the adverse effects of immunosuppressive regimens, primarily the susceptibility to infection as long as immunosuppression is applied. Cardiac and hepatic allografts would appear to employ very different procedures, they result in similar patterns of transplantrelated infection The reason for this apparent paradox is that the risk of infection is largely the result of the immunosuppressive treatment given to prevent acute and chronic rejection. This treatment is in principle standardized for all solid organ transplants.

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