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The human polyomaviruses BK (BKV) and JC (JCV) are ubiquitous in human populations and have a worldwide distribution.(1) They are oncogenic in rodents and monkeys and transform cells in vitro to a neoplastic phenotype. For all these reasons, BKV and JCV have been considered possible candidates in the etiology of human tumors. Association of BKV, but not of JCV, with human tumors has been described, although a formal proof for an etiological role of BKV in human oncogenesis is still lacking. SV40, which is not a ubiquitous human virus, has also been sporadically detected in human tumors. In this chapter, we consider their general characteristics, the natural history of infection, experimental transformation and oncogenicity by BKV and JCV, as well as the evidence linking BKV, JCV, and SV40 to human neoplasia.

Expression of cloned viral and cellular genes in eukaryotic cells is relevant to production of vaccines (Melnick, 1986; Moss and Flexner, 1987) and gene therapy (Anderson, 1984). To this purpose numerous eukaryotic vectors have been developed. Since the level of expression of exogenous genes is directly related to the degree of gene amplification (Rigby, 1983) episomal eukaryotic vectors have been constructed where a viral origin of replication directs vector amplification in suitable cells (DiMaio, 1987; Milanesi et al., 1984). However, only two eukaryotic vectors (Milanesi et al., 1984; Sugden et al., 1985) are specific for human cells and they allow expression of genes endowed with their own regulatory sequences. We have therefore devised a viral vector (pBK-1) that replicates and persists episomally in human cells; The structure and general characteristics of this vector have been described in detail (Milanesi et al., 1984). It contains DNA sequences from the plasmid pML, a deletion derivative of pBR322, as well as the origin of replication and the early region of BK virus (BKV), a human papovavirus that efficently replicates in human cells.