Antiviral treatment causes a unique mutational signature in cancers of transplantation recipients.

In post-HSCT clones with high mutation load and contribution of SBSA, C > A transversions demonstrated a highly significant Watson-versus-Crick-strand lesion segregation (false discovery rate [FDR] < 10e−12), which was absent in cells treated with KBrO 3 , deficient for OGG1 , and in HSPCs with a normal baseline mutation load (FDR = 0.17, 0.29, and 0.48, respectively; Figures 4 C, 4D, and S4 E).

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