Research progress in BK polyomavirus nephropathy

BK polyomavirus (BKPyV) typically enters host cells through caveolin-mediated endocytosis or clathrin-independent vesicle encapsulation, maintaining clinical latency without symptomatic manifestations. In immunocompromised hosts, particularly renal transplant recipients, viral reactivation within urothelial cells induces viruria, observed in 30%-40% of affected individuals. Subsequent retrograde viral migration along the urinary epithelium enables colonization of renal medullary tubules, establishing early-stage BKPyV nephropathy (BKPyVN). Progressive viral dissemination to cortical proximal tubules enhances replication kinetics, triggering cellular lyses and subsequent viremia in 10%-20% of cases. Persistent viral-induced cytopathology initiates cyclical epithelial damage and regenerative processes, ultimately manifesting as tubular atrophy, mononuclear inflammatory infiltration, and progressive interstitial fibrosis. This pathogenic cascade frequently culminates in irreversible allograft dysfunction and eventual graft failure.