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Epstein–Barr viral load as a marker of lymphoma in AIDS patients

✍ Scribed by Hongxin Fan; Seong Cheol Kim; Chukwuemeka O. Chima; Bruce F. Israel; Kathleen M. Lawless; Phyllis A. Eagan; Sandra Elmore; Dominic T. Moore; Steven A. Schichman; Lode J. Swinnen; Margaret L. Gulley

Publisher
John Wiley and Sons
Year
2004
Tongue
English
Weight
140 KB
Volume
75
Category
Article
ISSN
0146-6615

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✦ Synopsis

Abstract

Epstein–Barr virus (EBV) is implicated in the pathogenesis of acquired immunodeficiency syndrome (AIDS) lymphoma, and viral DNA is present within the malignant cells in about half of affected patients. We examined the extent to which EBV viral load is elevated in the plasma of AIDS lymphoma patients compared to AIDS patients with opportunistic infections. Sixty‐one AIDS patients were studied including 35 with lymphoma (24 non‐Hodgkin, six Hodgkin, and five brain lymphoma) and 26 with various opportunistic infections. In situ hybridization revealed EBV encoded RNA (EBER) expression in the malignant cells of 17/28 AIDS lymphomas (61%). In 232 serial plasma samples from 35 lymphoma patients and in 128 samples from AIDS controls, EBV viral load was assayed by quantitative‐polymerase chain reaction (Q‐PCR) using a TaqMan probe targeting the BamH1W sequence. EBV was detected in plasma from all 17 EBER‐positive AIDS lymphoma patients, with viral loads ranging from 34 to 1,500,000 copies per ml (median 3,210). Viral load usually fell rapidly upon initiation of lymphoma therapy and remained undetectable except in two patients with persistent tumor. In 11 AIDS patients, whose lymphoma lacked EBER expression, and in 26 control patients without lymphoma, levels of EBV in plasma were usually low or undetectable (range 0–1,995 and 0–2,409, median 0 and 0, respectively). There was no association between EBV viral load and human immunodeficiency virus (HIV) load or CD4 count. In conclusion, EBV viral load shows promise as a tool to assist in diagnosis and management of EBV‐related lymphoma patients. J. Med. Virol. 75:59–69, 2005. © 2005 Wiley‐Liss, Inc.

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