Figure 1

Association between the number of compensatory mutations, estimated fitness and clinical parameters. Compensatory mutations, polymorphic in subtype B protease and modeled by the fitness model F _PI , are likely candidates to explain the observed association of viral fitness estimated under drug selective pressure with clinical parameters. For patients with no indications of acute infection and TDR (n = 962), the number of compensatory mutations (13V, 36I, 60E, 62V, 63P, 71V, 71T, 77I or 93L) in the protease sequence is calculated for each patient [21]. The following parameters are grouped by mutation count: log₁₀ viral RNA copies/ml (1a), square-root transformed CD4 cell counts (1b) and increased estimated fitness for protease log₁₀F_PI−m(1c). The distribution of the respective parameter is shown for each group using boxplots. The horizontal line (bold) within the boxplot represents the median value, with box boundaries indicating the interquartile range. Upper and lower ends of striped lines denote the most extreme data point which is no more than 1.5 times the IQR range from the box. An increased mutation number significantly correlated with 1a) increased log₁₀ viral RNA copies/ml (p-value < 0.01), 1b) decreased square-root transformed CD4 cell counts (p-value < 0.01) and 1c) increased estimated fitness for protease log₁₀F_PI−m(p-value < 0.01). A fitted line going through the median values (lowess smooth) is shown in red. The number of patients for each group is shown above each bin.