Computational Biology Exposed a Common Pathogenic Mechanism in Influenza A and Guillain-Barré Syndrome

Influenza A (H1N1) is an acute respiratory infection, while Guillain-Barré syndrome (GBS) is an autoimmune peripheral neuropathy that can occur as a post-infectious complication. Clinical evidence suggests a potential link between H1N1 infection and subsequent GBS development, implying common immunopathological mechanisms. To explore this, we integrated bioinformatics and systems biology approaches to analyze transcriptome data from H1N1 and GBS patients in the GEO database, and 32 common differentially expressed genes (DEGs) were identified. Subsequent Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses revealed key functional associations for these DEGs. Protein-protein interaction (PPI) network analysis highlighted TLR4, TNF, and ITGAM as central hub genes, uncovering potential shared molecular pathways between H1N1 and GBS. Furthermore, analysis of hub gene interactions with microRNAs (miRNAs), transcription factors (TFs), and related diseases facilitated the prediction of potential therapeutic drugs. Molecular docking simulations were performed to validate predicted drug interactions with the hub gene products. Collectively, these findings delineate shared molecular mechanisms and provide insights for targeted therapy in patients developing GBS post-H1N1 infection.