Abstract
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. Single-cell 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. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00335-026-10194-8.