Kidney transplant recipients (KTRs) with impaired immune systems may develop BKV nephropathy (BKVN). BKVN and allograft rejection may harm transplanted kidneys. BKV replicates via miR-B1-5p and 3p in order to escape from host's immunological response. BKV alters KTR and viral gene expression and miRNA profiles. In an inflammatory setting, IFN-γ may initiate the removal of pathogens by inducing an immune response. It has antiviral immunity, which may prevent the virus from replicating by preventing the synthesis of BK virus proteins. Antiviral miRNAs like miR-29a are also produced in response to IFN-γ activation. Thus, we investigated these modifications as putative biomarkers for evaluating viral infection and the regulatory web that arises from their expression during infection and the emergence of post-transplant problems. This study was carried out on KTRs. Our research, which aimed to quantify and examine the amounts of cellular miRNA-29a, IFN-γ gene, BKV-miR-B1-5p and 3p from urine and blood in KT patient groups, has the potential to guide future research in the field. Patients with BKVN (BK-), patients without an active BKV infection (BK-), patients with a history of transplant rejection (Reject), patients without an active history of transplant rejection (Non reject), and a control group were among these groups. The Syber green real-time PCR was employed for the measurements and analysis. The findings of our investigation demonstrated that BK virus-caused kidney tissue damage (tissue), patients with an active BK virus infection (BK+), and KTRs who had previously experienced transplant rejection all showed less IFN-γ gene expression in comparison with control. These patients showed upper levels of miR-29a gene expression than the control group. Furthermore, these patients' gene expressions of miR-B1-5p and 3p showed higher in comparison with those of the control group. To date, there is no report on the effect of IFN-γ on the expression of BK polyomavirus miRNAs and related miRNAs in kidney transplant recipients with nephropathy compared to kidney transplant recipients without nephropathy in the Iranian population. Therefore, the results of this study can be used as a strategy to combat viral infections and pathogenesis caused by BK polyomavirus in kidney transplantation.