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Original Article

The Paul-Bunnell Heterophile Antibody Determinant in Epstein-Barr Virus-Associated Disease

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Pages 51-86 | Published online: 04 Dec 2011
 

Abstract

Reactivation of latent herpes viruses (notably Epstein-Barr virus, human herpesvirus-6) is commonly seen in chronic fatigue syndrome and it is believed to contribute to symptom perpetuation. Ep-stein-Barr virus (EBV), which was first isolated by Epstein, Barr and Achong (1964) from a cultured Burkitts's lymphoma lymphoblast cell line, is the etiological agent for infectious mononucleosis (IM), poly-clonal and oligoclonal lymphomas associated with primary and acquired immunodeficiencies, and the complications of X-linked lymphopro-liferative syndrome (XLP) (Cantani and Mastrantoni, 1989; Englund, 1988; Ernberg et al., 1990; Jones and Straus, 1987; Okano et al., 1988; Purtilo, 1987; Purtilo et al., 1981; Rowe et al., 1986; Saemundsen et al., 1981) and nasopharyngeal cancer (Pearson et al., 1984). Furthermore, people who have had IM have higher rates of subsequent development of malignant lymphoproliferative disorders (Abo et al., 1982; Snydman et al., 1982) and Hodgkins's disease (Green et al., 1979; Mueller, 1987; Poppema et al., 1985; Weiss et al., 1989), while patients with XLP have a higher incidence of non-Hodgkins's malignant lymphoma (Harrington et al., 1987). The precise role of EBV in these diseases or in CFS is not well understood. Nonetheless, it is known that EBV infection triggers the formation of heterophile antibodies that, for many decades, have formed the basis for serologic diagnosis of IM. In this review, we discuss the discovery, species variation, and structure of the erythrocyte membrane-associated Paul-Bunnell (PB) heterophile antibody determinant, its implications to IM diagnosis, and its potential contribution to defective immune surveillance, such as that seen in chronic fatigue syndrome.

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