Immunological control of virus-induced tumors in primates

Abstract

Cells infected by oncogenic viruses may transform, may develop a latent carrier state, or may be destroyed but understanding of the control of the results of infection is incomplete. Even if cells transform, ultimate development of a tumor may be immunologically controlled. For example, cells of some marmoset species transform after infection with RNA tumor viruses, and animals react to the transformed cells with cell-mediated and humoral immune responses. Both virus specific and cross-reacting cell membrane antigens have been demonstrated. Immune deficiency accelerates tumor growth or causes recurrence of a regressing tumor. In contrast certain simian herpesvirus (Herpesvirus saimiri, HVS and Herpesvirus ateles, HVA), which cause no or minor disease in their natural hosts, induce lymphomas or lymphoblastic leukemias in other primate species. The immune response of the natural host species to HVS is greater than that of animals developing malignancies after experimental infection. HVS and HVA share many properties with Epstein-Barr virus (EBV) of man, including antigens appearing early and late during infection and their related antibody responses but no evidence exists that they induce malignancies in their natural hosts. However, if induction is as infrequent as that with EBV and Burkitt's lymphoma (BL), we have not observed sufficient numbers of squirrel or spider monkeys to have seen a BL-like tumor. Interference with the immune systems of animals carrying HVS or HVA may induce tumor development, and clarify our understanding of the relationships between EBV and BL.