Human immunodeficiency virus (HIV) remains a worldwide health risk, having claimed over 35 million lives to date. No cure for HIV exists, and this is partially due to the virus’ high replication and mutation rate. Some of these mutations, termed viral adaptations, facilitate the virus’ evasion from an individual’s CD8+ T-cell response and detrimentally impact patient outcomes. Unfortunately, current HIV vaccine design approaches do not sufficiently incorporate viral adaptations, and it has become increasingly apparent through numerous unsuccessful clinical trials that these must be considered for an effective vaccine. Previous research has explored the detrimental impact of these adaptations in chronic HIV disease, yet further research is needed to understand the extent and functional impact of these adaptations during acute and early infection. Our study therefore analysed the CD8+ T-cell responses of 11 acutely infected individuals to established epitopes from various proteins in the HIV genome and corresponding viral sequencing, in order to explore the functionality of patient CD8+ T-cells and their impact on HIV viral adaptation. Using an IFN-γ enzyme-linked immunospot (ELISpot) assay and sequencing-based methods, we show that multiple proteins elicit a functional CD8+ T-cell response, yet only a small subset are consistently immunogenic across individuals. Moreover, we identify that numerous strong cellular responses to wildtype epitopes correspond to mutated epitopes in patient viral sequences, suggestive of strong CD8+ T-cell immune pressure during acute infection and rapid viral adaptation. Our research will aid current vaccine design prospects for HIV by improving the understanding of how quickly the virus can adapt in these early stages, which regions of the virus are more likely to adapt, and how these viral adaptations may reflect functional CD8+ T-cell responses.