1. ¹Department of Clinical Immunology, L Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland
2. ²Lower Silesian Center for Cellular Transplantation with Bone Marrow Donor Registry, Wroclaw, Poland

Correspondence: Professor K Bogunia-Kubik, Department of Clinical Immunology, L Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Rudolf Weigl 12, 53-114 Wroclaw, Poland. E-mail: bogunia@iitd.pan.wroc.pl

Received 20 December 2006; Revised 11 April 2007; Accepted 11 April 2007; Published online 28 May 2007.

Abstract

EBV reactivation is a serious complication affecting the recipients of allogeneic haematopoietic stem cell transplants (allogeneic HSCT). Recent reports have suggested that EBV reactivation induces increased expression of C-C chemokine receptor-5 (CCR5) or its ligands. Therefore, the 32-nucleotide deletion within the CCR5-encoding gene (CCR532 polymorphism) was analysed in 92 recipients of allogeneic HSCT and their donors and related with EBV load. In addition in 30 patients, at the same time points employing a real-time PCR technique, the number of viral copies and CCR5 transcripts were assessed. The incidence of EBV reactivation 2–3 months after transplantation was significantly lower in patients carrying the CCR532 allele (P=0.008). The association was confirmed in multivariate analysis, in which recipient CCR532 (OR=0.166, P=0.026) in addition to recipient age (OR=1.536, P=0.034) were identified as independent risk factors for EBV reactivation. Moreover, EBV reactivation was more frequently seen when patients and their donors were lacking the CCR5 deletion mutation as compared to other donor–recipient pairs (P=0.022). The CCR5 expression was significantly higher in the group of patients having EBV reactivation than in those lacking it (R=25.354, P=0.024). These results suggest that the expression of functional CCR5 plays a role in initiation/perpetuation of EBV reactivation.