Evidence map›Paper›PMID 39951298›Full record

ArticleInvestigative ophthalmology & visual science2025

kexB Gene Correlates With Aspergillus flavus Keratitis Severity: A Whole-Genome Analysis.

Jiamin Liu, Min Kang, Yuan Wei, Zijun Zhang, Jinding Pang, Qiankun Chen, Xizhan Xu, Zhenyu Wei, Yang Zhang, Kexin Chen and 3 more

Abstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Jiamin LiuBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Min KangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Yuan WeiBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Zijun ZhangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Jinding PangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Qiankun ChenBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Xizhan XuBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Zhenyu WeiBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Yang ZhangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Kexin ChenBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Zhiqun WangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Xinxin LuBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.
Qingfeng LiangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Fungal keratitis caused by Aspergillus flavus (A. flavus) can result in severe inflammation and corneal stromal melting, leading to visual impairment. This study aimed to identify virulent genes correlated with the severity of A. flavus keratitis using whole-genome sequencing. Methods: Whole-genome sequencing of 21 clinical A. flavus strains from cornea was performed to elucidate the pathogenesis of A. flavus in infectious keratitis, followed by pan-genome analysis and virulence analysis. To further understand the results from the previous analyses, growth phenotypes and virulence effect of mutant strains were validated experimentally, including the spore counting, growth pattern under different conditions, and clinical and pathological evaluation of A. flavus keratitis in mice models. Results: The A. flavus pan-genome was composed of 17,326 gene clusters with a core genome of 5378 (31.0% of the pan-genome) orthogroups in all 21 isolates. Virulence gene analysis revealed 183 genes contributing to A. flavus pathogenesis and mutation of the kexB gene was associated with the severity of keratitis. The kexB mutant (ΔkexB) strains showed significantly reduced conidia formation and lower growth rates in the presence of the cell-wall perturbing agents. Further, the mice models validated that clinical score, and corneal perforation rates significantly decreased in the group infected by ΔkexB strains. Infiltration of immune cells, gene expression of cytokines, and matrix metalloproteinase (MMP) were also decreased in the mutant group. Conclusions: The role of kexB gene in A. flavus keratitis was identified through whole-genome sequencing. Its mutation impairs conidia formation, cell wall integrity, and invasion, leading to milder clinical symptoms.

Indexed as

AspergillosisAspergillus flavusEye Infections, FungalFungal ProteinsKeratitisAnimalsDisease Models, AnimalFemaleGenome, FungalHumansMaleMiceMice, Inbred BALB CMutationSeverity of Illness IndexVirulenceFungal Proteins

Identifiers

PMID39951298
PMCPMC11824512

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.