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Thomas Hodgkin (1832) identified lymphoid neoplasia as a disease entity in man 146 years ago. His description served to focus attention on disorders arising within the lymphoid tissue as distinguished from those beginning elsewhere and only secondarily involving these areas. A very mixed assortment of diseases were first grouped together. Some were true lymphoid malignancies, others were not. In retrospect, at least three of Hodgkin’s original patients had tuberculosis rather than tumors (Fox, 1926). Nonetheless, the process of identifying lymphoid malignancies was begun. The subsequent sorting, describing, and classifying continues today.

Epstein-Barr virus (EBV) was discovered in 1964 (Epstein et al., 1964) and since that time an enormous amount has been learned about the biological and molecular attributes of this agent (Epstein and Achong, 1979a). In consequence, it is no longer difficult to explain how a unbiquitous virus that infects huge numbers of normal individuals in all human populations (W. Henle and Henle, 1979) is also both the cause of infectious mononucleosis (IM) in developed countries with high living standards (G. Henle and Henle, 1979), and involved in the induction, together with essential cofactors, of endemic Burkitt’s lymphoma (BL) (Epstein, 1978) and undifferentiated nasopharyngeal carcinoma (NPC) (Klein, 1979).

Herpesvirus saimiri (H. saimiri) is a ubiquitous agent of squirrel monkeys (Saimiri sciureus), a primate species native to the South American rain forests. The virus can easily be isolated from blood and tissue-culture cells of most healthy squirrel monkeys, and there is no evidence so far that H. saimiri is pathogenic in its natural host. After the first report on isolation of H. saimiri from primary kidney-cell cultures by Melendez et al. (1968) from the New England Primate Research Center, the virus was regarded as a harmless indigenous agent of squirrel monkeys. The interest in this virus arose from the observation that H. saimiri is extremely oncogenic in a number of other primate species that are presumably not infected under usual wildlife conditions (Melendez et al., 1969b). Marmoset monkeys of the genus Saguinus consistently develop malignant tumors of the lymphatic system, usually within 2 months of infection. The ability to induce neoplastic disease rapidly and reproducibly has made this system attractive for investigation of the biological, immunological, and molecular parameters of Cell transformation and tumor induction.

The early studies on the B virus (Herpesvirus simiae, herpesvirus B, simian herpesvirus, cercopithecine herpesvirus 1) are associated with the names of such pioneers in medical virology as Sabin and Wright (1934), Sabin (1934a-c), Burnet et al. (1939a,b), Melnick and Banker (1954), and Youngner (1956). In the 1930s, the virus was isolated and its cross-neutralization with herpes simplex virus (HSV) discovered. Some biological and morphological parameters were established in the 1950s. It was almost half a century, however, before the genetic material of the B virus could be characterized to allow for a clear differentiation from HSV and before the antigenic cross-reactivity with HSV and the bovine herpes mammillitis virus [bovid herpesvirus 2 (BHV-2)] could be pinpointed to major glycoprotein species (Sterz et al., 1973–1974; Ludwig et al.,1978; Norrild et al., 1978b; Pauli et al., 1981; and further details presented in this review).

Marmosets and tamarins, small monkeys native to Central and South America (Hershkovitz, 1966), have been used extensively in biomedical research during the past decade (Wolfe and Deinhardt, 1972; Deinhardt, 1973; Falk, 1974; Wolfe, Deinhardt, Ogden, Adams, and Fisher, 1975). In 1965, a nursery for hand-rearing neonatal marmosets was established in our laboratory, in conjunction with establishment of a breeding colony of marmosets for production of neonates for viral oncology studies. The nursery was required for rearing parentally neglected, uninoculated animals and animals inoculated with oncogenic viruses. Neonates were used in the experimental studies because of their greater susceptibility to selected oncogenic viruses and, once inoculated, were reared in isolation from the breeding colony to avoid contamination of the breeders and to permit closer monitoring for experimentally induced disease. Subsequently, hand-reared animals also were used in our laboratory in studies of slow virus diseases of the central nervous system.

The evidence pointing to a viral etiology for at least some forms of human cancer, a possibility that has long been considered on the basis of animal studies, has continued to accumulate to such an extent that viral oncologists must now reevaluate their clinical and experimental data in order to consider which specific approaches are now ready for clinical trials. Although ethical restrictions continue to inhibit attempts to prove that specific viruses cause certain human tumors, as outlined by Bryan et al. (1967; Bryan, 1962), epidemiological studies have been able to suggest not only which human tumors are most likely to be caused by infectious agents (Burkitt, 1962; Cole et al., 1968; Correa and O’Conor, 1971; Heath and Hasterlik, 1963; Kessler, 1974; Levine, 1974; Levine and Gravell, 1975; Morrow et al., 1971) but some have even suggested the pattern of the agents’ transmission (Kessler, 1976; Vianna et al., 1971).