Abstract

Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) is a critical immune checkpoint molecule involved in regulating T cell activation and tolerance. Genetic variations in CTLA-4 have been implicated in modulating susceptibility to human immunodeficiency virus (HIV) infection and disease progression. This review explores the impact of CTLA-4 genetic variations on HIV susceptibility, acquisition, transmission, and disease progression, as well as their potential implications for HIV prevention, treatment, and vaccine development. Despite conflicting results in studies across different populations, certain single nucleotide polymorphisms (SNPs) in the CTLA-4 gene have been associated with altered susceptibility to HIV infection. Moreover, CTLA-4 genetic variations have been linked to differences in viral load, CD4+ T cell count, and progression to AIDS in HIV-infected individuals. Mechanistically, these variations may influence immune activation, T cell function, cytokine production, and viral replication. Understanding the role of CTLA-4 genetic variations in HIV pathogenesis could lead to personalized treatment strategies and prognostication. Additionally, strategies targeting CTLA-4 may offer novel approaches for HIV prevention, immunotherapy, and vaccine development. Incorporating genetic information into HIV risk assessment and treatment decision-making may improve clinical outcomes and resource allocation in HIV care settings