Isolate-level pathogenic heterogeneity in keratitis caused by the Fusarium solani species complex: corneal invasion, host immunopathology, and model fidelity
8 affiliations
- 1The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, Henan, China
- 2Henan Academy of Innovations in Medical Science Eye Institute, Zhengzhou, Henan, China
- 3Department of Clinical Laboratory, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China
- 4Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China
- 5Beijing Aier-Intech Eye Hospital, Beijing, China
- 6The Third Affiliated Hospital of Henan Medical University, Xinxiang, Henan, China
- 7National Engineering Research Center for Ophthalmic Equipment, Beijing, China
- 8Beijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China
Abstract
Fungal keratitis caused by the Fusarium solani species complex (FSSC) often progresses despite antifungal therapy and can result in irreversible visual loss. Yet biological diversity within FSSC has not been integrated across taxonomy, isolate phenotype, corneal models, host response, and clinical outcome. This Review synthesizes taxonomic, experimental, and clinical evidence on isolate-level variation in adhesion, epithelial entry, stromal invasion, biofilm formation, tissue damage, immune activation, and antifungal response. Available data support substantial isolate-dependent heterogeneity but do not justify a stable species- or member-level ranking of clinical severity. Fungal developmental state, inoculation route, epithelial integrity, stromal architecture, host immunity, treatment timing, and tissue drug exposure all modify the phenotype observed. Cell, tissue, animal, and human-specimen models therefore provide complementary rather than interchangeable evidence, and few studies carry the same authenticated clinical isolate from corneal testing to longitudinal patient outcomes. Refractory FSSC keratitis is best investigated through a matched isolate–model–patient approach integrating multilocus authentication, spatial fungal localization, viable burden, host-mediated injury, compartment-specific drug exposure, and prespecified clinical endpoints. Such designs could distinguish persistent infection from inadequate tissue exposure and immunopathology and thereby improve risk stratification and therapeutic development.
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BibTeX
@article{he2026isolatelevel,
title = {{Isolate-level pathogenic heterogeneity in keratitis caused by the Fusarium solani species complex: corneal invasion, host immunopathology, and model fidelity}},
author = {Xin He and Ze Li and Shifei Wei and Yunyun Sun and Wenzai An and Qinyi Cui and Tao Wang and Qiuli Ming and Ningli Wang},
journal = {Frontiers in Cellular and Infection Microbiology},
year = {2026},
month = oct,
doi = {10.3389/fcimb.2026.1984688},
url = {https://doi.org/10.3389/fcimb.2026.1984688},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Isolate-level pathogenic heterogeneity in keratitis caused by the Fusarium solani species complex: corneal invasion, host immunopathology, and model fidelity
AU - Xin He
AU - Ze Li
AU - Shifei Wei
AU - Yunyun Sun
AU - Wenzai An
AU - Qinyi Cui
AU - Tao Wang
AU - Qiuli Ming
AU - Ningli Wang
PY - 2026
DA - 2026/10/22
JO - Frontiers in Cellular and Infection Microbiology
DO - 10.3389/fcimb.2026.1984688
UR - https://doi.org/10.3389/fcimb.2026.1984688
AB - Fungal keratitis caused by the Fusarium solani species complex (FSSC) often progresses despite antifungal therapy and can result in irreversible visual loss. Yet biological diversity within FSSC has not been integrated across taxonomy, isolate phenotype, corneal models, host response, and clinical outcome. This Review synthesizes taxonomic, experimental, and clinical evidence on isolate-level variation in adhesion, epithelial entry, stromal invasion, biofilm formation, tissue damage, immune activation, and antifungal response. Available data support substantial isolate-dependent heterogeneity but do not justify a stable species- or member-level ranking of clinical severity. Fungal developmental state, inoculation route, epithelial integrity, stromal architecture, host immunity, treatment timing, and tissue drug exposure all modify the phenotype observed. Cell, tissue, animal, and human-specimen models therefore provide complementary rather than interchangeable evidence, and few studies carry the same authenticated clinical isolate from corneal testing to longitudinal patient outcomes. Refractory FSSC keratitis is best investigated through a matched isolate–model–patient approach integrating multilocus authentication, spatial fungal localization, viable burden, host-mediated injury, compartment-specific drug exposure, and prespecified clinical endpoints. Such designs could distinguish persistent infection from inadequate tissue exposure and immunopathology and thereby improve risk stratification and therapeutic development.
SN - 2235-2988
ER -