Overview
- The peer-reviewed Science Advances paper from the University of York reports APOBEC-type DNA damage after BK virus exposure in human urothelium and in patient samples.
- The mutations arise from the host immune response rather than viral DNA integration, with damage also observed in neighbouring bystander cells.
- The proposed mechanism helps explain why many bladder tumors show no detectable viral traces at diagnosis years later.
- BK virus commonly infects in childhood, lies dormant in the urinary tract, and can reactivate under immunosuppression; kidney transplant recipients are reported to have more than triple the bladder cancer risk.
- Kidney Research UK and the research team say the findings open prevention-focused research paths to detect and control BK reactivation, though clinical guidance remains unchanged as work moves toward translation.