Epstein–Barr virus (EBV) infects >95% of the population worldwide.1 A small number of patients develop life-threatening persistence of high-level EBV replication following an infectious mononucleosis syndrome, often associated with splenomegaly and hepatitis.2 Chronic active EBV (CAEBV) disease is characterised by infiltration of tissues by EBV+ T, natural killer (NK) or less frequently B cells and can progress into lymphoproliferative disease. Clonal expansion of EBV-infected T or NK cells is well described.3

To date, CAEBV has been mostly described in Asian or South/Central American patients.4 Frequent deletions in the EBV genome have been found in samples from Japanese CAEBV patients (35%) and other EBV-driven neoplasms.5-7 However, it is unclear if these deletions are specific for Asian EBV strains, whether they are present in viral genomes in different sites and how they evolve overtime.

In the present study, we sequenced EBV from serial blood samples obtained from three UK patients with CAEBV disease. The results were compared with sequences from saliva of patients with CAEBV and blood and tissue from other benign and malignant EBV-related conditions.