Abstract
Epstein-Barr virus (EBV) genomes have been detected in peripheral blood lymphocytes (PBL) of patients with persistent polyclonal B-cell lymphocytosis (PPBL). This is consistent with the hypothesis that latent EBV infection is involved in the pathogenesis of this disorder. Two EBV-encoded proteins expressed in viral latency are the latent membrane proteins 1 and 2A (LMP1 and LMP2A). We have studied the LMP1 oncogene and the LMP2A gene in a female patient with PPBL and her five siblings. A cell line derived from peripheral blood lymphocytes (PBL) of the patient was also analyzed. A distinct 69-base pair deletion was identified within the carboxy terminal NF-κB activation domain of the LMP1 oncogene in PBL of the patient and in the cell line, whereas none of the siblings harbored this deletion. The tyrosine-signaling motif and the HLA A2.1 epitope of the LMP2A gene were wild type in the patient and all siblings. The presence of a 69-base pair deletion variant of the LMP1 oncogene within the lymphocytes of a PPBL patient but absence of this deletion variant in the unaffected siblings suggests a direct implication of altered LMP1 oncoprotein-dependent function in the pathogenesis of PPBL.
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Received: 26 August 1996 / Accepted: 24 October 1996
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Larcher, C., McQuain, C., Berger, C. et al. Epstein-Barr virus-associated persistent polyclonal B-cell lymphocytosis with a distinct 69-base pair deletion in the LMP1 oncogene. Ann Hematol 74, 23–28 (1997). https://doi.org/10.1007/s002770050250
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DOI: https://doi.org/10.1007/s002770050250