JCV is an opportunistic pathogen with a serological antibody positivity rate of more than 80% in the normal population. Initial infection usually occurs in childhood and is often asymptomatic, and JCV can be transmitted from mother to child through childbirth (placenta), breastfeeding, or prolonged shared contact, as well as through the respiratory and digestive tracts. After initial infection, JCV is present in human tissues in a latent state, but when host immunity is reduced, the virus can reactivate and replicate and cause pathological changes in the host. Morphologically, neither Decoy cell detection in urine nor renal tissue biopsy can distinguish BKV from JCV infection. Histologic features of JCV transplant nephropathy in Han Yong, National Institute of Organ Transplantation, 309th PLA Hospital include viral inclusion bodies in the nuclei of renal tubular epithelial cells, focal necrosis of renal tubular cells, and a large infiltration of inflammatory cells, often containing large numbers of plasma cells. The inclusion bodies are usually amorphous and basophilic hairy glass-like. Ultrastructural examination reveals crystalline-like arrangements of viral particles.The diagnosis of JC virus nephropathy includes: (i) characteristic pathologic changes in kidney biopsy specimens. (ii) Immunohistochemistry and in situ hybridization using specific JC virus DNA probes to detect BK virus in the kidney biopsy specimen. (iii) Microscopic observation of urine samples after histochemical staining. (iv) Qualitative PCR assay for BK virus DNA in plasma from patients with JC virus nephropathy using semi-nested primers. The combined use of these assays will greatly enhance the sensitivity, specificity, and disease prediction accuracy of the assay to 100%. Currently, there is no effective clinical treatment for PVAN and PML caused by JCV. The most important therapeutic measure is to rebuild the body’s immune function, and for kidney transplant recipients, the reduction or discontinuation of immunosuppressive drugs is beneficial for improving clinical symptoms. In addition, some progress has been made in domestic and international research, such as: ( 1) immunomodulatory therapy to increase the level of JCV-specific cytotoxic T lymphocytes, which may be a new way to solve the problem of PVAN and PML treatment [5]. ( 2) Anti-viral therapy: To date, no drugs have emerged that can specifically identify and kill JCV. A multicenter prospective study found that the combination of intravenous or intrathecal administration of cytarabine did not yield better clinical outcomes than highly active antiretroviral therapy (HAART) alone [7]. ( 3) Immunomodulatory therapy: Interferon-α, interferon-β, and interleukin-2 may help restore neurological functions damaged by PML. Serotonin-2α receptor blockers may prevent JC virus CNS and its dissemination. Such drugs include olanzapine, mirtazapine, ziprasidone, risperidone, etc. [8]. ( 4) Hematopoietic growth factors: interleukin 7 and recombinant human granulocyte colony-stimulating factor are able to accelerate lymphocyte maturation, and the combination of immunoglobulins can promote the body’s immune response to JCV [9]. ( 5) Drugs such as topoisomerase inhibitors may also play a therapeutic and preventive role in JCV-induced PVAN and PML [10]. early diagnosis of JCV is particularly important, and adopting an early diagnosis and treatment strategy can effectively prevent transplant kidney damage caused by JCV repopulation. In this study, we used real-time fluorescence quantitative PCR to detect JCV DNA concentrations in blood and urine samples from 89 subjects. Positive JC virus uropathy was detected in 17 cases (19.1%), and this incidence (19.1%) is consistent with reports from other foreign centers (13.7-36.8%) [9-13]. The median time to first viremia was 3 months after renal transplantation, and the mean time to first viremia reported by V. López [11] et al. was 2 ± 2.6 months after renal transplantation. The 89 subjects in this study did not develop JC viremia during follow-up, which may be related to the low incidence of JC viremia in renal transplant recipients and our small sample size. In a foreign trial of organ transplant recipients who participated in a trial comparing ganciclovir with valganciclovir in the prevention of cytomegalovirus (CMV) infection, JC viremia was detected in 4.9% of recipients. In contrast, in a study by V. López [11] and others on infections and nephropathy caused by polyomaviruses (BKV and JCV) in 76 renal transplant recipients, JC viremia was also not detected. In this study, we found that JC virus infection was more likely to occur in recipients who experienced acute rejection within 1 year after renal transplantation. It has been reported in the literature that some renal transplant recipients have suffered from tubular and uroepithelial damage due to acute rejection after surgery, which activates BK virus latent in the uroepithelium through “second strike” [12]. Since JC virus is in the same genus as BK virus, there are no reports on whether the “second strike” of acute rejection may also activate JC virus. Hormone shock is the most basic and effective treatment for acute rejection, and the immunity of the recipient will be temporarily and sharply reduced by hormone shock treatment. We believe that the “shock” of acute rejection and the dramatic drop in immunity caused by hormone shock therapy may activate and cause massive replication of the JC virus, and therefore this group of recipients has a higher incidence of JC virus urine disease. PVAN has a poor prognosis. The combined test can improve the diagnostic rate of PVAN, is simple, reliable and accurate, and lays the foundation for further research on the relationship between BK virus infection and graft loss after renal transplantation, which is an important guideline for the treatment of patients.