Saudi Journal of Kidney Diseases and Transplantation

ORIGINAL ARTICLE
Year
: 2006  |  Volume : 17  |  Issue : 3  |  Page : 351--354

Epstein-Barr Viral Infection in Renal Allograft Recipients: A Single Center Experience


Zakie Rostam Zadeh1, Khadije Makhdumi2, Shaker Salari Lak3,  
1 Department of Virology, Urmia Medical University, Iran
2 Department of Nephrology, Urmia Medical University, Iran
3 Department of Social Medicine, Urmia Medical University, Iran

Correspondence Address:
Zakie Rostam Zadeh
Assistant professor of Virology, Urmia Medical University
Iran

Abstract

In this study we attempted to identify the factors involved in Epstein-Barr viral (EBV) infection among renal allograft recipients. We studied 68 renal allograft recipients hospitalized at the Imam Khomeini Medical Center from 2001 to 2004. Blood samples were obtained from the patients before renal transplantation and repeated every 3 months during the first year after transplantation. Enzyme linked immunosorbant assay (ELISA) tests were performed on these samples to determine if antibodies to EBV antigens, such as viral capsid antigen(VCA)IgM, VCAIgG or Epstein Barr neoantigen (EBNA)IgG, were present. The types of prescribed immunosuppressive agents and the incidence of acute allograft rejection were closely observed to define their association with EBV. EBV infection developed in 58 (85.3 %) patients and active disease in 10 (14.7%). EBV was detected in 40 (58.8%) patients during the first year after transplantation. There was EBNAIgG seropositivity in 65 (95.6%) patients before transplantation; this number increased to 68 (100 %) after transplantation. In contrast, VCAIgG seropositivity increased from 92.6% before transplantation to 96.9% after transplantation; whereas VCAIgM seropositivity increased from 17.6% before transplantation to 58.8% after transplantation. There were no statistically significant differences in the reactivation of EBV infection between the different immunosuppressive regimens, between the groups of acute rejection and no acute rejection, or between the groups that received and did not receive anti-lymphocyte globulin (ALG) We conclude that most EBV activation after transplantation may represent a secondary form of a preexisting infection and we could not find a clear association with a specific immunosuppressive regimen, including the use of ALG. Further investigation is thus required to elucidate the factors involved in the reactivation of the EBV infection in the transplant population.



How to cite this article:
Zadeh ZR, Makhdumi K, Lak SS. Epstein-Barr Viral Infection in Renal Allograft Recipients: A Single Center Experience.Saudi J Kidney Dis Transpl 2006;17:351-354


How to cite this URL:
Zadeh ZR, Makhdumi K, Lak SS. Epstein-Barr Viral Infection in Renal Allograft Recipients: A Single Center Experience. Saudi J Kidney Dis Transpl [serial online] 2006 [cited 2022 Aug 19 ];17:351-354
Available from: https://www.sjkdt.org/text.asp?2006/17/3/351/35767


Full Text

 Introduction



Epstein Barr virus (EBV) causes a disease that can be intensified by the immunosuppressive agents used to prevent rejection of allografts.[1],[2],[3] Furthermore, active EBV infection can result in a dysfunction of the immune system that manifests itself as rejection or post-transplant lymphoproliferative disease (PTLD). [4]

EBV is one of the most prevalent viral infections. Studies have demonstrated that EBV is detectable in 80% to 90% of transplant recipients during the first year.[5]

The purpose of this study was to identify the manifestations of the EBV infection among renal allograft recipients.

 Methods and patients



We performed this study on 68 renal transplant recipients who were hospitalized at the Imam Khomeini Medical Center between 2001 to 2004. Blood samples were obtained prior to the operation and every three months during the first year post-transplant­ation. Enzyme linked immunosorbant assay (ELISA) tests were performed to determine if antibodies to EBV antigens, such as viral capsid antigen (VCA) IgM, VCAIgG or EBV neo-antigen (EBNA) IgG were present. The study patients' data included age, blood group, history of blood transfusion, and the cause of renal diseases. The immunosuppressive regimen and the episodes of allograft rejection were closely monitored.

Primary EBV infection was defined as seropositivity for VCAIgM; whereas previous EBV infection was defined as seropositivity for VCAIgG or EBNAIgG. Reactivation of EBV was defined as seropositivity for all VCA IgG, VCA IgM, and EBNA IgG.

 Statistical Analysis



We analyzed the collected data using the statistical package for social sciences software (SPSS). The X square values were compared and the statistical significance was set at P [4] Europe, [6],[7] and the U.S.A. [8]

Secondary active EBV infection was detected in 58.8% of our patients, which was higher than the 24.4% reported by Hornef et al, [8] the 27.7% reported by Rostamzadeh et al. [6] or the 17.7% reported by Kenagy et al. [9]

EBNAIgG, VCAIgG and VCAIgM were respectively positive in 95.6%, 92.6%, 17.6% of our patients prior to transplantation, and 100%, 96.9%, 58.8% during the first year after transplantation. Other studies detected a similar profile of antigens and antibodies. [6],[8],[9] Our results thus corroborate studies from other countries that indicate that EBV infection develops mostly as a secondary active disease after transplantation.

No particular immunosuppressive regimen was found to be responsible for the reactivation of EBV in our study, again in agreement with other studies. [6]

We did not find a statistically significant association between the incidence of infection and the occurrence of acute rejection in our study. The results of other similar studies [6],[8],[10] also indicate that acute rejection does influence EBV reactivation.

Furthermore, our results indicate that admini­stration of ALG after transplantation also did not influence EBV reactivation, again in agreement with other studies.[6],[8],[11]

In conclusion, our study suggests that most post-transplantation EBV activation is a secondary form of a previously existing infection. We could not detect a clear relationship with a specific immunosuppressive regimen or with the use of biological agents such as ALG. Further investigation is still needed to elucidate the factors involved in the reactivation of the EBV infection in the transplant population.

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