Epstein-Barr virus (EBV) is a human herpes virus that infects and immortalises B-lymphocytes. EBV is not only associated with infectious mononucleosis but also with malignant diseases such as Burkitt´s lymphoma and B-cell lymphoma. Development of tumours is a well-known complication in organ transplanted immunosuppressed patients. Most reports come from kidney transplantations and more recently studies from heart transplantations have been reported. It has been seen at Sahlgrenska University Hospital that 8 % of the heart/lung transplanted patients during the years 1988-1996 have developed an EBV induced lymphoid proliferation which can cause serious complications. This disorder is referred to Post Transplant Lymphoproliferative Disorder, PTLD. In order to find early markers for EBV associated tumours, specific EBV gene expression in B-cells in organ transplanted patients are studied. The EBV encoding protein EBNA 1 is expressed in all EBV infected cells and plays a major role in the replication of the virus DNA. EBNA 1 transcripts consist of several non-coding mRNA regions. One of these RNA regions, encoded by the U-exon in the EBV genome is missing in the EBNA 1 transcript detected in transplanted patients with PTLD. In this work we wanted to characterise the function of the U-exon. This was done by constructing EBV cDNA expression vectors with the Luciferase reporter gene. The constructs were used to transfect three different human cell lines, Rael, P3HR-1 and DG-75 in order to analyse the luciferase expression in constructs with or without RNA sequences corresponding to the U-exon. RT-PCR experiments were used in an attempt to find out which promotor was used, and to see if there could be a new start for transcription in the U-exon. We have found that the presence of the U-exon up regulates the expressional level by several times. The RT-PCR analysis showed that no new initiation of transcription is located in the U-exon. Our data indicate that presence of the U-exon have an influence on the Fp activity.