The δ-retrovirus genus includes human T-cell leukemia viruses (HTLV-1, HTLV-2, HTLV-3), simian T-lymphotropic viruses (STLV), and bovine leukemia viruses (BLV), which establish lifelong, typically asymptomatic, infections. However, HTLV-1 and BLV can lead to leukemia or lymphoma in 2-5% of infected hosts after prolonged latency. HTLV-1, the first identified human oncogenic retrovirus, drives T-cell leukemia/lymphoma via cell-intrinsic mechanisms. Similarly, BLV induces B-cell lymphoma in cattle, sharing key genomic and disease progression features with HTLV-1. Retrovirus-induced leukemias/lymphomas arise through complex interactions of viral and host factors. This review explores current virological perspectives on δ-retroviral oncogenesis, focusing on proviral integration sites within the host genome. Additionally, we briefly compare HTLV-1 with the human immunodeficiency virus (HIV), highlighting that while HIV causes AIDS, it also induces clonal expansion of infected cells. Finally, we discuss the potential diagnostic and prognostic value of analyzing viral factors and integration sites.
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