A cry for help from leaf to root: above ground insect feeding leads to the recruitment of rhizosphere microbes for plant self-protection against subsequent diverse attacks.

Polyomavirus nephropathy (BKPyVAN) is a major cause of allograft dysfunction after kidney transplantation (KTX). While plasma BKPyV-PCR is the diagnostic gold standard, it may not fully reflect tissue injury. We conducted a prospective observational proof-of-concept study in 30 KTX recipients with BKPyV reactivation (November 2022-February 2024); 21 underwent kidney biopsy, 11 were diagnosed with biopsy-proven (BP)-BKPyVAN. Urine samples were analyzed by flow cytometry to quantify the potential of VP1-positive reno-urinary epithelial cells as a novel non-invasive marker of active tubular damage. The control cohort included 21 virology-negative patients. Median urinary VP1-positivity was higher in BP-BKPyVAN (33%, IQR 27-46) vs. non-BKPyVAN patients (5%, IQR 1-13; p < 0.001). The assay achieved an AUC of 0.98 (95% CI 0.93-1.00, p = 0.0003; cut-off: 11.7%; sensitivity = 91%, specificity = 89%) for BP-BKPyVAN. Longitudinally, median VP1-burden declined from 13% (IQR 4-29) at baseline to 0% (IQR 0-0.4). BKPyV-DNAemia declined rapidly, but plateaued at ∼4 × 102-7 × 102 copies/mL, whereas urinary VP1-positive cells became undetectable. Our preliminary results suggest that combining urinary VP1-positivity with plasma BKPyV-PCR may help distinguish BP-BKPyVAN from non-BKPyVAN within a BKPyV-reactivation cohort. Longitudinal VP1 tracking may indicate resolution of viral infection earlier than DNAemia. These findings are hypothesis-generating and require validation in larger independent cohorts.