Exploring the impact of interferon-gamma single nucleotide polymorphisms on HTLV-1 infection: Unraveling genetic influences in viral pathogenesis.

Human T-lymphotropic virus-1 (HTLV-1) induces neoplastic adult T-cell leukemia/lymphoma (ATLL) and neurological HTLV-1 associated myelopathy (HAM) in approximately 3 %-5 % of infected individuals. The precise factors that facilitate disease manifestation are still unknown; interaction between the virus and the host's immune response is key. Cytokines regulates physiological activities and their dysregulation may initiate the pathogenesis of various malignant and infectious diseases. Genetic variations, particularly polymorphisms in gene regulatory regions, lead to varying cytokine production patterns. Interferon-gamma (IFN-γ), a key cytokine in HTLV-1 infection, is a signature cytokine for T-helper 1 (Th1) cells that interferes with viral replication and enhances innate and adaptive immune responses during viral infections. The IFNG gene possesses several single nucleotide polymorphisms (SNPs), among which the + 874 A/T SNP has been widely studied for its functional role in HTLV-1 infection. The purpose of this review was to provide insight into the impact of IFNG SNPs on HTLV-1 Infection.