Interestingly, we found that B*57/*58-positive patients with the compensatory mutations had significantly higher viral loads and lower CD4 cell counts than those without the compensatory mutations (Figure 3), indicating that the proposed mechanism of virus attenuation by the escape mutation and its restoration by the compensatory mutations at the B*57/*5801 TW10 epitope is applicable in the context of CRF01_AE infections. Here, CD4 is linked to infection.