Introduction: Kidney transplantation is the preferred treatment for children with end-stage renal disease, yet it needs lifelong immunosuppressive therapy to prevent graft rejection. Balancing immunosuppression to prevent rejection while avoiding drug toxicity and overimmunosuppression remains challenging. Current dosing relies on plasma drug levels, which inadequately reflect individual immune status. This gap in personalized monitoring elevates risks of infection, rejection, and post-transplant lymphoproliferative disease. Therefore, additional biomarkers are essential to better assess immune function in pediatric kidney transplant recipients. Previous studies performed in adult kidney transplant recipients have shown that plasma levels of Alphatorquevirus, including Torque teno virus (TTV), hold promise as immune activity marker, where high TTV loads indicate a reduced immune activity. TTV is part of the Anelloviridae. The human “anellome” contains not only TTV but also Betatorquevirus, and Gammatorquevirus.This study aims to assess how the anellome changes in children post-transplantation, hypothesizing (1) that anelloviruses will be introduced with the donor kidney and (2) that donor anelloviruses may colonize and persist in the recipient. 
Methods: Six donor-recipient pairs were analysed, including three living-unrelated (LUR) and three living-related (LR) pairs. Recipients were monitored from before transplantation and up to two years post-transplantation (median age = 15.1 years (2.93 – 17.5), median number of samples = 6.5 (2 - 11)), donors were measured one time before transplantation. DNA from serum or plasma was analysed using quantitative Polymerase Chain Reaction (qPCR) and Rolling Circle Amplifications, Illumina library preparation, and SCANellome V2 to study the anellome. 
Results: Three out of six donors (LUR) tested positive for anelloviruses, allowing comparison with the composition and development of the anellome in recipients. One recipient, who was on immunosuppressive therapy before transplantation, showed high anelloviral DNA (>10¹⁰ copies/mL) from start. One donor-derived anellovirus lineage was identified in one recipient. No donor lineages were detected in the other recipients. However, additional lineages became detectable in recipients.  
Conclusion: Donor-derived anellovirus was identified in one paediatric recipient, possibly due to transmission or reactivation of a pre-existing lineage, suggesting a more compromised immune status. No donor-derived lineages were detected in the other recipients. However, additional lineages became detectable in all recipients, making it uncertain whether these originated from the donor or were already pre-existing but undetectable in the recipient. These findings indicate that TTV transmission is seen in a minority of paediatric kidney transplant recipients.