Initial infection with BKV is usually acquired in childhood, mostly asymptomatic or manifesting as a mild flu-like illness.In the setting of immunosuppression, the virus reactivates and begins to replicate, triggering renal tubular cell lysis and viruria.In patients with kidney transplants, reactivation of BKV typically reaches peak incidence at 3 months post-transplantation with BK viral replication in the kidney graft, causing BKV-associated nephropathy (BKVAN), which manifests as kidney dysfunction that may result in eventual loss of the transplanted kidney. Reactivation of BKV in the bladder can lead to hemorrhagic cystitis.