Vitamins as modulators of Deltaretrovirus infection: implications for HTLV-1 and bovine leukemia virus-associated diseases

Deltaretroviruses, particularly human T-cell leukemia virus type 1 (HTLV-1) and bovine leukemia virus (BLV), are oncogenic retroviruses responsible for severe lymphoproliferative and inflammatory diseases, including adult T-cell leukemia/lymphoma (ATLL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Despite decades of research, effective curative therapies remain limited, and disease progression is strongly influenced by host immune and metabolic factors. Accumulating evidence indicates that vitamins play critical roles in modulating viral pathogenesis, immune dysregulation, oxidative stress, and tissue damage in Deltaretrovirus infections. Clinical, experimental, and genetic studies demonstrate that deficiencies or altered signaling of vitamins D, C, and B complex are associated with increased disease susceptibility, inflammatory severity, and neurological or hematological complications in HTLV-1-infected individuals. Vitamin D signaling, in particular, has been linked to immune regulation, control of proviral load, and genetic susceptibility via vitamin D receptor polymorphisms. Antioxidant vitamins, such as vitamin C, exert pro-apoptotic effects in HTLV-1-transformed cells, while vitamin B derivatives improve neurological function and quality of life in HAM/TSP patients. Emerging data also suggest parallels in BLV infection, including vitamin-related metabolic alterations and potential zoonotic implications. This review synthesizes current evidence on the role of vitamins in Deltaretrovirus infection, highlights mechanistic and clinical insights, and identifies critical knowledge gaps. Understanding vitamin-dependent pathways may support the development of adjunctive, low-cost strategies to improve disease outcomes in HTLV-1- and BLV-associated disorders.