*Purpose: Human Polyomaviruses (HPyV) infections are extremely common, ranging from 60% to 100% in the general population, depending on the virus. After primary infection, which mostly occurs asymptomatically during childhood, HPyV can establish life-long latency in renal tubular epithelial cells. Immunosuppression is a well recognized risk factor for HPyV reactivation and in kidney transplant (KTx) recipients it may favor the development of clinically significant HPyV-related diseases such as nephropathy or leukoencephalopathy. It has been demonstrated that HPyV can be transmitted by the donor or it can be latent in the recipient, reactivating when the net state of immunosuppression is increased. However, exact origin, replication pattern, and clinical significance of clinically silent HPyV infections after KTx remain unclear.

*Methods: A total of 630 specimens (urine, blood, and allograft biopsy) were collected from 58 KTx donor/recipient pairs. Sampling was carried out immediately before transplant and periodically from 1 to 900 days after surgery. Specimens were tested for BK Polyomavirus (BKPyV), JC Polyomavirus (JCPyV), Merkel Cell Polyomavirus (MCPyV), Human Polyomavirus 7 (HPyV7), and Human Polyomavirus 9 (HPyV9) genome by virus-specific duplex TaqMan Real Time PCR. Viral strains were molecularly characterized by automatic sequencing.

*Results: Median follow-up was 486 (119-900) days. HPyVs viruria was present in 29/58 (50%) donors and 43/58 (74%) recipients. JCPyV DNA was detected in 26/58 (45%) donors and in 23/58 (40%) recipients; 18/58 (31%) donor/recipient pairs showed identical JCPyV strains. BKPyV DNA was detected in 3/58 (5%) donors and 18/58 recipients (31%) whereas MCPyV genome was detected in 2/58 (3.5%) donors and 15/58 (26%) recipients. Median time from KTx to first detectable replication of JCPyV, BKPyV and MCPyV reactivation was 1 (0-398), 81 (0-375) and 98 (0-544) days post KTx, respectively. HPyV replication in kidney biopsies confirmed viruria data. Based on the association results, JCPyV infection was protective against BKPyV, but not MCPyV infection (p<0.05). One patient developed nephropathy associated to BKPyV/JCPyV coinfection.

*Conclusions: JCPyV reactivation occurred in the early post KTx phase and was mostly due to strains transmitted by the donor. MCPyV and BKPyV replications occurred at a later stage and, in the majority of patients, were due to reactivation of recipient strains or primary infections. JCPyV replication occurring during the first weeks post KTx seems to prevent BKPyV reactivation/infection. Systematic screening for HPyV replication after KTx could help discriminate recipients at increased risk of virus-related complications.

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