Abstract

Abstract Background and Aims The role of polyomaviruses (PyV) in malignancy is controversial, this can be demonstrated in three ways; Firstly, hit and run mechanism where polyomaviruses contribute to the early phases of oncogenic progression. The second way, where PyV act as a passenger as polyomaviruses neither necessary nor contribute to the oncogenic progression. The third way, where PyV acts as (bystander) as PyV is not related to the malignancy, but PyV could be detected in the anatomically connected sites or neighbouring cells. BKV has been classified as a possible carcinogenic to humans (2b) as there is sufficient evidence that it is carcinogenic to animals, however, BKV carcinogenicity evaluation to humans was inadequate. There are inconsistent data regarding the contribution of BKV to tumors that occur in both animals and humans. Method Retrospective analyses of 492 consecutive renal transplant recipients in a single-center, 2010-2018. Data Source: prospectively managed electronic patient records. Malignancy data in both control and BKV infected groups were assessed. Results A total of 492 cases were studied, were categorized into 2 groups the BKV infected group (n:73) patients and BKV non-infected group (n: 419) patients, then an assessment of different malignancies in both groups. The BKV infected group had 15 cases out of 73 who had malignancy, while the BKV non-infected group had 28 cases out of 419 totally (Table 1). The association between malignancy in BKV was statistically significant (P-value of 0.038). Moreover, the risk factors involved in the development of malignancy in renal transplant recipients were older age, BK virus infection and maintenance immunosuppression agents (Table 2). Lastly, Logistic regression analysis was used to assess predictors of malignancy among renal transplant recipients. For every one-year increase in age among renal transplant recipients, the odds of having a malignancy increase by 4.6% (p=0.003). Meanwhile, there is a 4 times increase in the odds of having malignancy for recipients who are BK virus-positive vs. those who are BK virus negative (p=0.001). Furthermore, there is a 10 times increase in the odds of having malignancy for recipients who are on sirolimus as a maintenance immunosuppressant vs. those who are on TAC/PRED/MMF (p=0.007). Conclusion Our study highlights the statistically significant correlation between BK virus infection and the development of malignancy in renal transplant recipients. However, statistical correlation doesn`t mean causation which makes the potential oncogenic role of BKV is unclear. Also, there is increased reporting of malignancy in patients infected with BKV. Increased vigilance is required for early detection of malignancy in patients infected with BKV not only the patients who are heavily immunosuppressed.

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