Acute T-lymphoproliferative syndromes are caused by herpesvirus saimiri (HVS) and ateles in neotropical primates; by alcelaphine herpesvirus-1 and ovine herpesvirus-2 strains in domestic cattle and other ungulates; and by the α-herpesvirus of Marek's disease in chickens. T-cell lymphoproliferation caused by these herpesviruses has short incubation periods and a rapid course when compared with retroviral disease. The B-lymphotropic Epstein–Barr virus (EBV) is also associated with some human T-cell malignancies. Analogous to EBV in B cells, HVS isolates of the subgroup C are uniquely capable of transforming human and Old World primate T lymphocytes to continuous growth in cell culture and can provide useful tools for T-cell immunology or gene transfer. Signal transduction pathways stimulated by the viral oncoproteins seem to converge at related cellular effector proteins, in total providing a proproliferative signal. However, the viral oncoproteins most likely evolved to evade immune recognition and to support persistent infection in the natural host, where these viruses are frequently apathogenic.