The Role of CMV and EBV in Renal Allograft Loss


To the Editor:

I read with interest the study by Bamoulid et al. [1] looking at the incidence and consequences of Epstein–Barr virus (EBV) viremia in renal transplant recipients. Their study is to be commended for further elucidating the natural course of EBV in adult renal transplant recipients. Unsurprisingly, EBV reactivation after transplant was associated with a higher occurrence of opportunistic infections, likely reflecting the degree of immunosuppression. Interestingly, the authors also found an association between EBV reactivation and graft loss even when controlling for confounding factors. Interstitial fibrosis/tubular atrophy accounted for more than half of the graft losses in their study.

It is worth noting that the EBV reactivation group had a higher incidence of cytomegalovirus (CMV) disease (defined as CMV viral replication and symptoms), although this was not statistically significant. The authors did not report the frequency of CMV viremia in the EBV reactivation group. A previous study showed that CMV viremia (with a viral load greater than or equal to 2000 copies/mL) was associated with an increased risk of interstitial fibrosis/tubular atrophy of renal transplant recipients 3 months after transplantation [2]. CMV viremia may therefore be an important confounding factor in this study contributing to allograft loss. Inclusion of this variable in the final regression model would further help us understand the relative effect of EBV and CMV in renal allograft loss.

  • R. J. S. Arasaratnam*

  • Department of Internal Medicine

  • University of North Carolina

  • Chapel Hill, NC

  • *Corresponding author: Reuben J. S. Arasaratnam,


The author of this manuscript has no conflicts of interest to disclose as described by the American Journal of Transplantation.