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. 2008 Apr 2;82(11):5594–5605. doi: 10.1128/JVI.02356-07

FIG. 5.

FIG. 5.

Model summarizing forces that influence selection of the escape mutations in the B27-KK10 epitope. The relative influence of CTL escape mutations in the KK10 epitope on HLA-B27 binding, in vitro viral replication, and predicted in vivo viral replication capacity in the presence of KK10-specific CTL is illustrated. Viral sequences in the KK10 epitope are shown on the left, and mutations at residue 264 are indicated in red or blue text. The ability of the WT KK10 peptide (yellow) or KK10 P2 variants (red) to bind to HLA-B27 is classified as strong, weak, or very weak based on data presented in Fig. 3. In the panels on the right, in vitro and putative in vivo replication capacities of WT (black), R264K (red), R264T/G/Q (collectively in blue), and SARKLM (green) are displayed. The dashed line represents the hypothesized in vivo replication “threshold” that may need to be overcome for a given variant to dominate the quasi-species.