Given that the NPN3A mutation was associated with a numerically diminished response following infection with either the wt or NPN3A influenza A viruses (Fig 2) , we also asked if there was any effect on CD8 + T cell function or phenotype, particularly for markers (CD62L and CD127) that discriminate between memory T cell subsets [27, 28] . More of the D b NPN3A + CD8 + T cells remained CD62L hi when sampled at the peak of the response (d10) following primary challenge (Fig S1A) , confirming the impression from the quantitative analysis (Fig 2 A-C) that there may be less clonal expansion. On the other hand, IL-7R expression was comparable for the D b NPN3A + CD8 + and D b NP 366 + CD8 + T cell populations generated in virus-infected naïve mice (Fig S1 CD) with both being (p,0.01) lower than the values for the D b PA 224 -specific set ( Fig S1C) . This suggests that IL-7R levels may be antigen dose-rather than magnitude-dependent. Neither of these differential effects was apparent for d28 memory T cells specific for the mutant or wt epitopes (Fig S1BD) . Functional analysis of cytokine production based on short term (5h) stimulation with cognate peptide in the ICS assay showed no obvious differences at any stage for the D b NP 366 and D b NPN3Aspecifc T cells, though the usual divergence [29] from the D b PA 224 + CD8 + T cell response was observed (p,0.01) (Fig S1 E-H) . These data suggest that NPN3A mutation leads to crossreactive, but diminished, CD8 + T cell responses with comparable cytokine production profiles.