Possible immunological mechanisms in C-type viral leukemogenesis in mice.

Abstract

C-type viruses are etiologically associated with a variety of neoplasms in several different species (Tooze 1973). In general, two distinct mechanisms of pathogenesis appear to be involved. In all sarcomas and a variety of lymphomas, directly oncogenic, acute transforming viruses are involved. These viruses can directly cause transformation both in vivo and in vitro and transformation is due to the presence of oncogenic sequences acquired by the virus from genomic sequences. In most cases, the acquisition of transforming sequences results in the deletion of viral sequences required for replication, resulting in a replication defective virus requiring a “helper” virus for these functions. The mechanisms by which C-type viruses induce the more general forms of leukemia, however, appear to be quite distinct from those associated with sarcomas. First, the viruses involved are replication competent, nontransforming, and do not contain additional cellular sequences associated with pathogenesis. Second, unlike sarcomas and other acute viral diseases, the latencies associated with leukemogenesis are from 3 to 12 months in contrast to 10–14 days. Third, the ability of C-type viruses to induce leukemia in most cases is associated with and requires an acute state of viremia. Last, more recent data have demonstrated that the majority of leukemias are monoclonal tumors (Steffen and Weinberg 1978; Canaani and Aaronson 1979; Neiman et al. 1980). Therefore, leukemogenesis appears to be a result of rare events occurring over long periods due to extensive, viral replication.