Staphylococcus aureus leads a dual lifestyle: it is both a common commensal, colonising the nasal passages of up to 60% of the population, and a major cause of bloodstream infections. Nasal colonisation is a significant risk factor for subsequent infection, with patients often infected by their own microbiome strains. Previous genomic studies have shown high genetic relatedness between colonising and infecting isolates within the same patient, suggesting short evolutionary timescales during the transition from commensalism to pathogenicity. This raises key questions about the genetic mechanisms driving infection and the functional relevance of infection-associated single nucleotide polymorphisms (SNPs). Using a collection of over 300 S. aureus isolates, we phenotypically characterised and compared infection-associated (I) and nasal (N) strains from the same patients to identify signatures of the commensal-to-pathogen switch. Prior genotyping revealed enrichment of SNPs in infection isolates, particularly in genes regulated by the global virulence regulators rsp and agr, and in genes encoding proteins responsive to host-derived antimicrobial peptides. To assess the phenotypic impact of these mutations, we systematically compared growth dynamics, biofilm formation, and haemolytic activity between paired I and N strains. Our results reveal notable phenotypic variability across isolates, with greater divergence correlating with increasing genetic distance. However, virulence-associated phenotypes clustered primarily by clonal complex (CC), rather than by isolate source (I vs N). These findings suggest that S. aureus virulence potential is largely lineage-dependent, with no major in vitro shift in virulence observed between carriage and infection states.