Influenza A Virus is responsible for over 500,000 deaths annually and causes significant mortality and morbidity during pandemics. Due to the rapid mutation of the virus’s surface glycoproteins, vaccines are revised and administered annually. Despite Australia’s annual effort to provide free vaccines to 4.5 million at-risk individuals (infants and elderly), many are still hospitalised. It is well-established that possessing a diverse influenza-specific T cell receptor (TCR) correlates with improved T-cell polyfunctionality and disease protection. Traditionally, influenza-specific CD8+ T-cell responses have been studied in adults with the highly prevalent HLA-A*0201 (HLA-A2) allele, which presents the conserved Influenza A Virus Matrix Protein peptide M158-66 (GILFTVFTL). Here, we investigate the evolution of HLA-A2-M1-specific TCRs in individuals of three distinct age groups: infants (cord blood), adults and the elderly. A TRBV19 bias was observed in all HLA-A2-M1-specific T-cell populations, especially in adults (78%) and elderly (78%), but decreased in infants (36%). Interestingly, the most prevalent public TRBV19 clonotypes identified in adults were diminished in elderly, and instead, distinct TRBV19 clonotypes were observed. This suggests that repeated influenza exposure over time influences the composure of the TCR repertoire and may indicate T-cell exhaustion of the public TRBV19 clonotype over time. By solving the structure and measuring the binding affinity between several age-dependent TCR-HLA-A2-M1 complexes, this study aims to elucidate the way in which T-cell exhaustion may alter TCR repertoires. These findings could potentially contribute to the restoration of cytotoxicity for exhausted CD8+ T cells in the elderly and inform the development of T cell-based therapies for personalised medicine.