The effect of human leukocyte antigen A1 and B35‐Cw4 on sustained BK polyomavirus DNAemia after renal transplantation

Abstract

BK polyomavirus (BKPyV) is a known cause of nephropathy in renal allograft recipients. Reactivation of latent BKPyV infection causes significant viruria in 30%-40% of renal transplant patients. 1,2 Subsequently, one third of patients with BKPyV viruria develop DNAemia, which indicates more extensive replication and damage to the allograft. 3 BKPyV DNAemia may progress to significant fibrosis of the renal allograft and tubular atrophy known as polyomavirus-associated nephropathy (PyVAN). 3,4 PyVAN is unfortunately associated with 10%-100% graft loss rate. 5,6 Human leukocyte antigen (HLA) class I presentation pathway plays a central role in alerting the immune system to virally infected cells. 6,7 Recognition of HLA class I molecules is required for the