HIV infects and depletes CD4+ T cells leading to severe immunosuppression. Currently almost 38 million people live with HIV worldwide. Rare individuals, termed HIV controllers, can control viral load and remain healthy while infected. Despite Human Leukocyte Antigen (HLA) gene diversity in the population, almost 50 % of HIV controllers express the HLA-B57 molecule which presents, among others, the Gag derived epitope, TW10. Strong T-cell responses to this epitope result in escape mutations in TW10 that reduce the viral fitness. Given its presentation in early infection, TW10, could therefore shape the long-term control of HIV. However, the mechanisms contributing to HIV control related to this epitope remain unclear. Here, we study the CD8+ T cell responses to the TW10 epitope presented in HLA-B*57:01+ HIV+ individuals. We determine the αβ T cell receptor (TCR) repertoire in both HIV controller and non-controller individuals revealing similarities and the existence of a public TCR and public clonotypes in both groups. We further determine the polyfunctionality and avidity of selected T cell clones from each group that reveal strong CD8+ T cell responses, shaped by the specific TCR repertoire biases regardless of the viral load. Furthermore, affinity measurements of selected TCRs and the first crystal structure of HLA-B*57:01-TW10 in complex with a CD8+ TCR reveal the molecular basis of TW10 recognition. The link between HIV viral load and T cell function driven by immunodominant epitopes may further our understanding of immunologic control of HIV.