Figure 2.
TCR repertoire restoration in relation to CMV serostatus and infection/reactivation. Stratification according to the following groups: seronegative (n = 20), seropositive (n = 21), and reactivated (n = 13) CMV recipients applies to plots (A-E). (A) Evolution of TCR-productive Simpson clonality at serial time points after HSCT fitted using LOESS regression with a 95% confidence interval. (B) Productive frequency distribution at 12 months after HSCT with respect to groups. (C) TCR repertoire overlap computed using the Morisita-Horn index between 3 and 12 months after HSCT. Morisita-Horn indices vary between 0 (no overlap) and 1 (complete overlap) and are represented along the y-axis. (D) Private (upper panel) (ie, observed in only 1 D/R pair) and public (lower panel) (ie, observed in ≥2 D/R pairs or matching clonotypes present in public databases with antigen-specific validated TCRs) fractal clonal size organization at serial time points after HSCT. Each bar represents a single individual. The color-coded legend bar represents the stratification according to the individual clone’s productive frequency. (E) Cumulative productive frequency of CMV–specific TCR clones identified by in silico matching with public databases at serial time points after HSCT. (F) Cumulative productive frequency of donor-recipient nonshared and shared (ie, between each D/R pair) CMV-specific TCR clones in D–/R+ (n = 9) and D+/R+ (n = 4) CMV reactivated recipients at all time points combined. The cumulative frequencies at each time point are detailed in supplemental Figure 4A. Box plots display medians and IQRs, with whiskers representing 1.5× IQR. Wilcoxon-rank sum test for pairwise comparisons in panels B,F. All P values were 2-sided. Statistical thresholds: ∗P < .05; ∗∗P < .01; ∗∗∗P < .001.