Timothy Dambaugh

Biochemistry of Epstein—Barr Virus

The objective of this introduction is to develop concisely the context in which biochemical studies of Epstein—Barr virus (EBV) have been undertaken. Elements of history and biology are relevant to an understanding of the somewhat unusual course of biochemical research with EBV.

Persistence and Expression of the Epstein-Barr Virus Genome in Latent Infection and Growth Transformation of Lymphocytes

Epstein-Barr Virus (EBV) is believed to be an important etiologic agent of nasopharyngeal cancers (NPC) especially of the anaplastic type since (i) NPC cells invariably harbor EBV (Wolf et al., 1975; Huang et al., 1974; Klein et al., 1974); (ii) EBV is believed to be a cause of human B lymphocyte tumors (Epstein and Achong, 1978); (iii) the immune response to EBV infection is predictive of NPC development and of prognosis (Henle et al., 1970; Zeng et al., 1980; Pearson et al., 1984); and (iv) most NPC tumors originate from an unique anatomic site where there is closest proximity between lymphoid cells in which EBV is latent and epithelial cells in which tumor originates (Prasad 1981). Because of difficulties in infecting epithelial cells with EBV and in propagating NPC cells in vitro, current knowledge of EBV-induced cell proliferation comes mostly from the human B-lymphocyte tumor model. Not only is EBV almost always present in burkitt lymphoma cells (Nonoyama et al., 1973; Lindahl et al., 1974); nut also, virus infection of lymphocytes in vitro leads to cell proliferation (Henle et al., 1976; Pope et al., 1968), virus-infected cells from tumors in nonhuman primates (Miller et al., 1977), and virus-transformed cells of varying stages of oncogenic potential can be grown in continuous culture (Nilsson 1971).