ArticleGenome medicine2026
Identification and functional characterization of regulatory variants in DPP9 associated with COVID-19 severity.
Article in Genome medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed.
- Identifying severe COVID-19 risk variants modulating enhancer reporter activity in lung cells.PLoS genetics · 2026Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leads to a wide-range of clinical outcomes, which have been extensively studied through genome-wide association studies (GWAS).
methodsStarting from lead genetic variants associated with COVID-19 infection and severity, we identified a subset of non-coding candidate variants with potential regulatory functions. We combined bioinformatics analysis and functional screening in three cell lines to provide evidence for regulatory activity. We then performed a genetic study to test the association of our selected candidates with disease susceptibility followed by the functional validation of the risk haplotype.
resultsWe prioritized two DPP9 variants within a haplotype that increases the risk of severe COVID-19. This haplotype exhibited increased regulatory activity and altered transcription factor binding, suggesting its role in influencing COVID-19 severity by modulating DPP9 expression in immune and lung cell types.
conclusionsThe interest of our study lies in the functional characterization of regulatory variants responsible for increased levels of DPP9 and lung damage observed in patients with severe COVID-19. These findings advance our understanding of genetic risk factors for COVID-19 and highlight functional SNPs that may guide future therapeutic research.
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