Exploration of shared gene signatures and molecular mechanisms between psoriasis and COVID-19: evidence from transcriptome data
et al., Mammalian Genome, doi:10.1007/s00335-026-10194-8, Jan 2026
In silico study showing shared molecular mechanisms between COVID-19 and psoriasis through transcriptomic analysis. Authors identified 66 common upregulated genes between the two conditions, with eight hub genes (OAS2, MX1, IRF7, RSAD2, OASL, IFIT1, IFIT3, and ISG15) showing high diagnostic accuracy (AUC >0.7 for COVID-19, AUC >0.9 for psoriasis).
Dong et al., 13 Jan 2026, China, peer-reviewed, 4 authors.
Contact: yyeli2000@126.com, youwanglu@163.com.
Exploration of shared gene signatures and molecular mechanisms between psoriasis and COVID-19: evidence from transcriptome data
Mammalian Genome, doi:10.1007/s00335-026-10194-8
Emerging evidence suggests that the onset or worsening of psoriasis can occur following COVID-19 infection or vaccination. Additionally, individuals with psoriasis may be more susceptible to COVID-19. However, the underlying mechanisms driving this phenomenon remain unclear. This study aims to explore the potential shared mechanisms and the complex interplay between psoriasis and COVID-19. Gene expression profiles for COVID-19 (GSE162183) and psoriasis (GSE54456) were obtained from the Gene Expression Omnibus (GEO) database. Common differentially expressed genes (DEGs) were identified, followed by functional annotation, protein-protein interaction (PPI) network construction, and hub gene identification. Validation of hub genes was performed using independent datasets (GSE152075 and GSE157103 for COVID-19; GSE121212 and GSE78097 for psoriasis). Receiver operating characteristic (ROC) curves were used to assess the predictive value of the hub genes. Gene set enrichment analysis (GSEA) and immune infiltration analysis were conducted, and expression patterns of the hub genes were further explored using a single-cell RNA sequencing dataset. A total of 66 common DEGs (all upregulated) were identified. The influenza A and NOD-like receptor signaling pathways were enriched in both COVID-19 and psoriasis. OAS2, MX1, IRF7, RSAD2, OASL, IFIT1, IFIT3, and ISG15 were identified as hub genes after validation, with all are under the curve (AUC) > 0.7 for COVID-19 and AUC > 0.9 for psoriasis. Upregulation of these hub genes was associated with increased infiltration of neutrophils and Th17 cells. Singlecell analysis showed that the hub genes were primarily expressed in epithelial cells in COVID-19 and keratinocytes in psoriasis. This study reveals shared pathogenic mechanisms between psoriasis and COVID-19 and provides insights into how COVID-19 may exacerbate psoriasis. The identified common pathways, hub genes, and associated cell types offer valuable guidance for future research and potential therapeutic targets.
Author contributions Conceptualization, Data curation, YWL; Formal analysis, YWL; Funding acquisition, YYL, RJD, and YWL; Investigation, Methodology, LHY; Supervision, YYL; Visualization, Writing -original draft, RJD; Writing -review & editing, all authors.
Declarations Conflict of interest The authors declare no competing interests.
Ethical approval Not applicable. Consent to participate Not applicable.
Consent for publication Not applicable. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit h t t p : / / c r e a t i v e c o m m o n s . o r g / l i c e n s e s..
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