Bioinformatics analysis and initial validation of potential therapeutic targets for COVID-19 infection in osteoarthritis patients

Abstract Background The emergence of severe coronavirus disease 2019 (COVID-19) and its ensuing complications presents a substantial challenge to human safety. Osteoarthritis (OA) stands as the most common degenerative joint disease, while the intricate molecular relationship between OA and COVID-19 remains enigmatic. In this investigation, we employed systematic bioinformatics analysis to uncover the underlying molecular mechanisms associated with these two diseases. Additionally, we identified potential therapeutic drugs with the potential to aid in the treatment of patients afflicted with both COVID-19 infection and osteoarthritis (OA). Methods Datasets for both COVID-19 and OA were sourced from the GEO database. Subsequently, a differential expression analysis was executed to procure Differentially Expressed Genes (DEGs). Co-expressed genes shared between OA and COVID-19 were identified through the intersection of differential gene sets, employing a Venn diagram. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by Metascape. The hub genes were identified through protein-protein interaction (PPI) analysis carried out in Cytoscape, and their validity was subsequently affirmed through brief experiment. Finally, transcription factor-gene interactions, microRNA (miRNA) candidate identification and drug candidate identification were identified by co-expression of genes. Results A total of 94 co-expressed DEGs were obtained. GO and KEGG enrichment analysis of DEGs showed that they mainly affect inflammation, cytokine and immune-related functions, and inflammation-related signaling pathways. Through the analysis of the PPI network, we obtained 9 hub genes, and validated them with brief experiments. In addition, the top ten drug candidates ranked by P-value were screened, which may exhibit potential for providing therapeutic benefits in the context of treating individuals affected by both COVID-19 infection and OA. Conclusion This study reveals a shared molecular mechanism between osteoarthritis (OA) and neocoronary pneumonia. Additionally, it clarifies potential mechanisms linked to synovial lesions in both neocoronary pneumonia and osteoarthritis. These shared pathways and hub genes might offer insights for future investigations.