Enhancement of Epstein-Barr virus replication in producer cell lines by a combination of low temperature and corticosteroids

Abstract

Epstein-Barr virus (EBV) is a ubiquitous virus of man which, after infection, persists in a latent state throughout the life of the individual (1). Acute infection may be clinically inapparent, or it may result in infectious mononucleosis, a self-limiting disease (2). In addition, EBV DNA is almost invariably detected in the tumor cells of African patients with Burkitt’s lymphoma and patients throughout the world with nasopharyngeal carcinoma (3, 4). In both cases, epidemiological studies strongly suggest that the malignant disease arises some years after acute infection with EBV (5, 6). However, while EBV can induce tumors in primates (3, A), a causal relationship with human malignancy has not been established. Since DNA virus replication leads to cell death, tumor cells, or the cells of continuous cell lines which contain EBV, are of necessity either nonpermissive or minimally permissive with respect to EBV replication (1,7,8). The capacity of DNA viruses to persist in a latent state is thus inextricably bound up with their potential oncogenicity, and studies of the mechanism of latency are therefore of considerable interest. In the case of EBV, an additional, more pragmatic reason for the study of latency is the lack of a fully permissive in vitro culture system, with resultant difficulty in obtaining sufficient quantities of virus for biochemical and other studies. Factors exist which may influence the transcription of certain cellular as well as