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Peer-reviewedCC BYEmerging microbes & infections

HLA profiles and susceptibility to Alveolar echinococcosis: evidence from a large cohort with population and household controls.

  • Lynn Peters1
  • Zuotang Ye1
  • Alexander Grunenberg1
  • Giuseppe Zenatti1
  • Wanjie Jiang1
  • Yasemin Özkan1
  • Nele Wellinghausen2
  • Teresa Rangel-Vivar2
  • Benedikt Haggenmüller3
  • Andreas Binzberger4
  • Wolfgang Kratzer4
  • Marko Kornmann5
3 more authors
  • Erik Rasbach5
  • Daniel Fürst6,7,8
  • Beate Grüner1
8 affiliations
  1. 1Department of Internal Medicine III, Division of Infectious Diseases, University Hospital Ulm, Ulm, Germany.
  2. 2Department of Infectious Disease Immunology and Allergology, MVZ Labor Ravensburg GbR Labor Dr. Gärtner, Ravensburg, Germany.
  3. 3Department of Radiology, University Hospital Ulm, Ulm, Germany.
  4. 4Department of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
  5. 5Department of General and Visceral Surgery, University Hospital Ulm, Ulm, Germany.
  6. 6Institute of Clinical Transfusion Medicine and Immunogenetics Ulm, German Red Cross Blood Transfusion Service, Baden Wuerttemberg - Hessen, Germany.
  7. 7University Hospital Ulm, Ulm, Germany.
  8. 8Institute of Transfusion Medicine, University of Ulm, Ulm, Germany.
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Abstract

Alveolar echinococcosis (AE) is an emerging and potentially fatal helminthic disease. Despite widespread environmental contamination with infective Echinococcus multilocularis (EM) eggs in endemic areas, human AE remains rare, suggesting an important role of host genetic susceptibility. In this case-control study, HLA variation was assessed by amplicon-based next-generation sequencing in 360 patients with AE and compared with (i) 1,440 population controls matched, where feasible, on age, sex, and place of residence, and (ii) 100 unrelated household controls to account for shared environmental exposure to EM. Analyses included age- and sex-adjusted Firth-penalized logistic regression, linkage disequilibrium (LD)-aware haplotype analyses, simulation-based maximum-score tests, and Benjamini-Hochberg false discovery rate correction. At two-field resolution, C*07:01 was associated with increased AE odds (OR 2.10; adjusted p = 0.006), whereas B*18:01 was associated with reduced odds (OR 0.49; adjusted p = 0.014). Haplotype analyses identified an extended LD-defined background involving A*29, C*16, or both, frequently combined with B*44, DRB1*07, or DQB1*02. A*29 carriage corresponded to the A01-A24 supertype category. A*29-DQB1*02 remained significant after within-model and study-wide correction (OR 3.92; adjusted p = 0.005 and 0.039, respectively), while C*16-B*44-DQB1*02 remained significant after within-model correction (OR 2.83; adjusted p = 0.041) but not after study-wide correction. Exploratory analyses of early-onset AE (≤35 years; n = 63) suggested associations with A*31:01 (OR 2.86) and DQB1*05:03 (OR 3.44), although neither remained significant after multiple-testing correction. These findings support a contribution of individual HLA alleles and extended haplotypic backgrounds to AE susceptibility within a multifactorial host-environment model.

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Cite

BibTeXRIS
BibTeX
@article{peters2026profiles,
  title = {{HLA profiles and susceptibility to Alveolar echinococcosis: evidence from a large cohort with population and household controls.}},
  author = {Lynn Peters and Zuotang Ye and Alexander Grunenberg and Giuseppe Zenatti and Wanjie Jiang and Yasemin Özkan and Nele Wellinghausen and Teresa Rangel-Vivar and Benedikt Haggenmüller and Andreas Binzberger and Wolfgang Kratzer and Marko Kornmann and Erik Rasbach and Daniel Fürst and Beate Grüner},
  journal = {Emerging microbes \& infections},
  year = {2026},
  month = oct,
  doi = {10.1080/22221751.2026.2744492},
  url = {https://europepmc.org/article/MED/42876258},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - HLA profiles and susceptibility to Alveolar echinococcosis: evidence from a large cohort with population and household controls.
AU  - Lynn Peters
AU  - Zuotang Ye
AU  - Alexander Grunenberg
AU  - Giuseppe Zenatti
AU  - Wanjie Jiang
AU  - Yasemin Özkan
AU  - Nele Wellinghausen
AU  - Teresa Rangel-Vivar
AU  - Benedikt Haggenmüller
AU  - Andreas Binzberger
AU  - Wolfgang Kratzer
AU  - Marko Kornmann
AU  - Erik Rasbach
AU  - Daniel Fürst
AU  - Beate Grüner
PY  - 2026
DA  - 2026/10/15
JO  - Emerging microbes & infections
DO  - 10.1080/22221751.2026.2744492
UR  - https://europepmc.org/article/MED/42876258
AB  - Alveolar echinococcosis (AE) is an emerging and potentially fatal helminthic disease. Despite widespread environmental contamination with infective Echinococcus multilocularis (EM) eggs in endemic areas, human AE remains rare, suggesting an important role of host genetic susceptibility. In this case-control study, HLA variation was assessed by amplicon-based next-generation sequencing in 360 patients with AE and compared with (i) 1,440 population controls matched, where feasible, on age, sex, and place of residence, and (ii) 100 unrelated household controls to account for shared environmental exposure to EM. Analyses included age- and sex-adjusted Firth-penalized logistic regression, linkage disequilibrium (LD)-aware haplotype analyses, simulation-based maximum-score tests, and Benjamini-Hochberg false discovery rate correction. At two-field resolution, C*07:01 was associated with increased AE odds (OR 2.10; adjusted p = 0.006), whereas B*18:01 was associated with reduced odds (OR 0.49; adjusted p = 0.014). Haplotype analyses identified an extended LD-defined background involving A*29, C*16, or both, frequently combined with B*44, DRB1*07, or DQB1*02. A*29 carriage corresponded to the A01-A24 supertype category. A*29-DQB1*02 remained significant after within-model and study-wide correction (OR 3.92; adjusted p = 0.005 and 0.039, respectively), while C*16-B*44-DQB1*02 remained significant after within-model correction (OR 2.83; adjusted p = 0.041) but not after study-wide correction. Exploratory analyses of early-onset AE (≤35 years; n = 63) suggested associations with A*31:01 (OR 2.86) and DQB1*05:03 (OR 3.44), although neither remained significant after multiple-testing correction. These findings support a contribution of individual HLA alleles and extended haplotypic backgrounds to AE susceptibility within a multifactorial host-environment model.
SN  - 2222-1751
ER  -