PRF1 and infection: This loss of cytotoxic potential over time can at least partially be explained by a change in the relative expression levels of T-bet and Eomes: HIV-specific cells were equally T-betHiEomes+ and T-betLoEomes+ during acute infection and both subsets efficiently upregulated perforin initially but the proportion of T-betLoEomes+ cells increased significantly as infection progressed and cells with this phenotype had an inferior capacity to express perforin compared to T-betHiEomes+ cells.