Serologic and molecular diagnosis of epstein-barr virus infections

Abstract

Epstein-Barr virus (EBV), a member of the herpesvirus group, was isolated from cultured Burkitt's lymphoma (BL) cell lines in 1964 (2). EBV is a ubiquitous virus that may be the most widely disseminated human virus, affecting more than 95% of the world population. Additionally, EBV is the causative agent of infectious mononucleosis (IM) and is associated with certain human malignancies, such as BL and nasopharyngeal carcinoma (NPC) (1, 2, 6-8). EBV-associated lymphoproliferative lesions also occur in both primary and acquired immunodeficiency disorders (6-8). Chronic active EBV infection is another category of EBV-related disorders, which recently has been described in persons without clearly defined underlying disease (6, 7). Significant differences prevail in the prevalence and age-specific incidence of primary infection in persons among geographic areas and socioeconomic groups in any given country (1). Most primary EBV infections, transmitted through saliva, occur during childhood in Africa, Asia, and developing countries, and result in a subclinical infection (1, 6, 8). In contrast, persons residing in North America, Europe, and most other developed countries are frequently seronegative for EBV antibodies until adolescence, and two-thirds of newly seroconverted persons of this age group manifest with IM (1, 6, 8). In vitro, EBV infects B lymphocytes of humans and some primates, and lifelong latency develops (2, 6, 8). Defenses against EBV infection include mucus, epithelial barriers, interferon, neutralizing antibodies, EBV-specific and non-EBV-specific activation of cytotoxic T cells, and antibody-dependent cell-mediated cytotoxicity (6, 8). The clinical and pathophysiological manifestations of the infection are chiefly due to the enlargement of lymphoid tissues caused by the proliferation of infected B cells and reactive T cells (6, 8). Also cellular infiltration of liver, brain, bone marrow, and other organs can induce lesions and dysfunction. Herein, we describe our approach to serologic and molecular studies to document EBV infection.