Skip to main content
. 2010 May 5;84(14):7018–7028. doi: 10.1128/JVI.00548-10

FIG. 5.

FIG. 5.

(A) Intracellular IFN-γ staining analysis of ES1 HLA-B27 tetramer-positive cells to autologous and wild-type KK10 (KRWIILGLNK; Gag 263-272) peptides. (B) IFN-γ ELISPOT analysis of ES8 CD8+ T cells to autologous TW10 variants and wild-type TW10 peptide (TSTLQEQIGW; Gag 240-249). (C) IFN-γ ELISPOT analysis of ES31 CD8+ T cells to autologous TW10 variant and wild-type TW10 peptides. (D) IFN-γ ELISPOT analysis of the ES7 CD8+ T cells to the wild-type and the autologous peptide containing the K335R mutation in DL15 (DCKTILKALGPAATL; Gag 329-343). (E) Magnitude of IFN-γ response by ES8, ES3, ES7, and ES9 to four epitopes in which evolution occurred in the plasma virus of either ES7 or ES8. Data reflect the IFN-γ response to the autologous variant of the epitope of each patient at the latest time point available. Open symbols indicate SFC < 50. Circles indicate the response by patients in whom no evolution was seen in this epitope, while diamonds indicate the response by the patient in whom the evolution of the plasma virus occurred in this epitope (ES8 for TW10 and ES7 for IW9, QW9, and KF11).