# HLA‐B Leader Dimorphism Predicts BK Polyomavirus Replication After Kidney Transplant

**Authors:** Aurélien Aubry, Baptiste Demey, François Helle, Ophélie Fourdinier, Julien Lion, Judith Desoutter, Etienne Brochot, Nicolas Guillaume

PMC · DOI: 10.1111/tan.70477 · Hla · 2025-11-20

## TL;DR

This study finds that a specific HLA-B gene variation may predict BK virus replication in kidney transplant patients.

## Contribution

The study identifies HLA-B leader dimorphism as a potential predictor of BK polyomavirus replication after kidney transplantation.

## Key findings

- HLA-B leader mismatch between donor and recipient is protective against BKPyV replication.
- No significant association was found between HLA-B leader dimorphism and CMV replication.
- HLA-B leader dimorphism could be a useful predictor of BKPyV risk if confirmed in other studies.

## Abstract

BK polyomavirus (BKPyV) and Cytomegalovirus (CMV) often replicate after kidney transplantation, with management limited to reducing immunosuppression and risking rejection. Among genetic factors that may modulate the antiviral response, HLA evolutionary divergence (HED, allowing a greater diversity of antigen presentation) and the HLA‐B leader dimorphism (MM, MT, TT, influencing NK cell–mediated immunity) are interesting. We aimed to compare these parameters between patients who experienced viral replication within the first post‐transplant year and those who did not. We analysed 306 kidney transplants performed between 2019 and 2023 at Amiens University Hospital. HLA typing was performed in recipients and donors to determine HED (loci A, B, C, DRB1, DQB1) and HLA‐B leader dimorphism. 22.5% of the recipients (69/306) developed BKPyV possible nephropathy (defined by urinary PCR > 7 log10 copies/mL or DNAemia) and 40.2% (123/306) developed CMV infection during the first year. In a multivariate analysis, a donor–recipient HLA‐B leader mismatch was protective against BKPyV replication (OR = 0.48; p = 0.02), whereas no similar association was observed for CMV replication (OR = 1.42; p = 0.169). HLA‐B leader dimorphism could serve as a predictor of BKPyV replication risk, if confirmed in independent cohorts.

## Linked entities

- **Genes:** HLA-B (major histocompatibility complex, class I, B) [NCBI Gene 3106], HLA-A (major histocompatibility complex, class I, A) [NCBI Gene 3105], HLA-C (major histocompatibility complex, class I, C) [NCBI Gene 3107], HLA-DRB1 (major histocompatibility complex, class II, DR beta 1) [NCBI Gene 3123], HLA-DQB1 (major histocompatibility complex, class II, DQ beta 1) [NCBI Gene 3119]

## Full-text entities

- **Genes:** HLA-DRB1 (major histocompatibility complex, class II, DR beta 1) [NCBI Gene 3123] {aka DRB1, HLA-DR1B, HLA-DRB, SS1}, HLA-DQB1 (major histocompatibility complex, class II, DQ beta 1) [NCBI Gene 3119] {aka CELIAC1, HLA-DQB, IDDM1}, HLA-A (major histocompatibility complex, class I, A) [NCBI Gene 3105] {aka HLAA}, HLA-B (major histocompatibility complex, class I, B) [NCBI Gene 3106] {aka AS, B-4901, HLAB}
- **Diseases:** nephropathy (MESH:D007674), HED (MESH:D005099), CMV infection (MESH:D003586)
- **Species:** Homo sapiens (human, species) [taxon 9606], Betapolyomavirus hominis (species) [taxon 1891762], Cytomegalovirus (genus) [taxon 10358]

## Full text

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## Figures

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## References

34 references — full list in the complete paper: https://tomesphere.com/paper/PMC12634932/full.md

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Source: https://tomesphere.com/paper/PMC12634932