Fig. 2: CMV is associated with divergent CD8+ T cell transcriptomic and clinical response to ICB.
a, cICB treatment of CMV− patients leads to a highly significant induction of CMV score (y axis) (top-left panel), not observed in CMV− patients receiving sICB (bottom-left panel) (n = 79 CMV−, n = 72 CMV+; P = 2.8 × 10−9 cICB CMV−, P = 0.28 sICB CMV−, P = 0.41 cICB CMV+, P = 0.54 sICB CMV+). P values derived from two-sided Wilcoxon signed-rank test; lower and upper box hinges represent the 25th to 75th percentiles, the central line represents the median and the whiskers extend to the highest and lowest values no greater than 1.5 × IQR. b, cICB treatment leads to a significant induction of cytotoxicity score irrespective of CMV status (n = 64 CMV− P = 2.1 × 10−7, n = 44 CMV− P = 0.0013). P values derived from two-sided Wilcoxon signed-rank test; boxplot as in a. c, Kaplan–Meier analysis shows no significant difference in OS of cICB-treated CMV+ and CMV− patients (n = 113 CMV−, n = 78 CMV+; P = 0.92, two-sided log-rank test). d, Kaplan–Meier analysis demonstrates increased OS of CMV+ versus seronegative sICB recipients (n = 30 CMV−, n = 45 CMV+; P = 0.039, two-sided log-rank test). e, Cox proportional hazards model as per d shows significantly reduced adjusted HR for death in CMV+ recipients of sICB (HRadj = 0.37; 95% CI, 0.18 to 0.78; P = 0.0089, Wald test). Increased age is significantly associated with increased risk of death when controlling for CMV (HRadj = 1.07; 95% CI, 1.02 to 1.13; P = 0.0058, Wald test). f, Improved PFS in stage II/III resectable patients following sICB in CMV+ patients relative to CMV− patients (n = 11 CMV−, n = 17 CMV+; P = 0.030, two-sided log-rank test).
