Bioinformatics Analysis of Key Expressed Genes and Potential Therapeutic Targets in Parvovirus B19 Infection and Rheumatoid Arthritis

Objective To identify the core genes linking human parvovirus B19 (B19V) infection and rheumatoid arthritis (RA) using bioinformatics methods, providing new insights into etiology and targeted therapy.Methods The B19V-infected and control dataset (GSE103460) and the RA patient and healthy control dataset (GSE55235) were downloaded from the GEO database. Differentially expressed genes (DEGs) for B19V infection and RA were identified separately using R language. The intersection of DEGs from both diseases was taken to obtain common genes (co-DEGs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the co-DEGs. A protein-protein interaction (PPI) network was constructed using the STRING database and visualized with Cytoscape to screen for hub genes.Results A total of 772 DEGs (411 up-regulated, 361 down-regulated) were identified in the B19V gene expression profile, and 1,413 DEGs (781 up-regulated, 632 down-regulated) were identified in the RA gene expression profile. The intersection revealed 104 key co-DEGs associated with both B19V and RA. Enrichment analysis indicated that these co-DEGs were significantly involved in pathways related to viral infectious diseases, immune cell differentiation (Th17 cell differentiation), inflammatory signaling (TNF, PI3K-Akt), and various cancers. Finally, the top 10 hub genes were identified based on the Maximal Clique Centrality (MCC) algorithm via the CytoHubba plugin: JUN, FOS, EGR1, DUSP1, FOSB, PTGS2, MYC, CDKN1A, ZFP36, and JUNB.Conclusion This bioinformatics study identifies 10 core genes, including JUN, FOS, EGR1, DUSP1, and FOSB, that are commonly associated with both B19V infection and RA. These genes are primarily enriched in inflammatory stress and immune regulation processes related to pathways such as immune cell differentiation and inflammatory signaling, providing new clues and potential therapeutic targets for elucidating the molecular mechanism by which B19V infection contributes to RA pathogenesis.