BK polyomavirus infection is the important cause of virus-related nephropathy following kidney transplantation. BK virus reactivates in 30%–80% of kidney transplant recipients resulting in BK virus-related nephropathy in 1%–10% of cases. Currently, the molecular processes associated with asymptomatic infections in transplant patients infected with BK virus remain unclear. In this study we evaluate intrarenal molecular processes during different stages of BKV infection. The gene expression profiles of 90 target genes known to be associated with immune response were evaluated in kidney graft biopsy material using TaqMan low density array. Three patient groups were examined: control patients with no evidence of BK virus reactivation ( ), infected asymptomatic patients ( ), and patients with BK virus nephropathy ( ). Analysis of biopsies from asymptomatic viruria patients resulted in the identification of 5 differentially expressed genes (CD3E, CD68, CCR2, ICAM-1, and SKI) ( ), and functional analysis showed a significantly heightened presence of costimulatory signals (e.g., CD40/CD40L; ). Gene ontology analysis revealed several biological networks associated with BKV immune control in comparison to the control group. This study demonstrated that asymptomatic BK viruria is associated with a different intrarenal regulation of several genes implicating in antiviral immune response. 1. Introduction Innovations to immunosuppressive regimens have improved patient and kidney transplant survival rates; however, drug-induced immune suppression has also resulted in significant increases in complications associated with infections. BK polyomavirus (BKV) infections have emerged as an important cause of virus-related nephropathy following kidney transplantation in the era of modern immunosuppressive therapies [1]. BKV has been shown to reactivate in 30%–80% of kidney transplant recipients but only in 1%–10% of cases resulted in the development of BKV nephropathy (BKVN) associated with subsequent kidney graft deterioration and failure [2–5]. Recently, the polymerase chain reaction (PCR) has been used for routine monitoring of BKV replication in peripheral blood [5]. However, PCR screening has demonstrated that a majority of kidney transplant recipients are BKV positive in urine but not blood and never develop BKV nephropathy with graft function deterioration. Furthermore, it was shown that patients with asymptomatic viruria presented with significant BKV viral loads in kidney graft biopsy specimens [6], suggesting successful control of the BKV infection by the host
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