Computational Biology Exposed a Common Pathogenic Mechanism in Influenza A and Guillain-Barré Syndrome
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Background
Influenza A (H1N1) is an acute respiratory infection caused by influenza viruses, while Guillain-Barré syndrome (GBS) is an autoimmune peripheral neuropathy that can arise as a post-infectious complication. The existence of clinical evidence indicates that patients afflicted with influenza A may concomitantly develop Guillain-Barré syndrome (GBS). This observation suggests the presence of a shared immunopathological mechanism.
Methods
This study integrates bioinformatics analysis and experimental validation strategies to systematically identify common differentially expressed genes (DEGs) from H1N1 and GBS transcriptomic datasets. By constructing protein-protein interaction (PPI) networks, hub genes were screened, followed by comprehensive analysis of their regulatory networks (including miRNA/TF interactions) and disease associations. Finally, drug prediction and molecular docking experiments were performed to validate the reliability of the identified targets.
Results
The analysis yielded 32 common differentially expressed genes (DEGs). The PPI network analysis identified TLR4, TNF, and ITGAM as key hub genes. The application of functional enrichment analysis has yielded the identification of potential common pathways between influenza A (H1N1) and GBS. Furthermore, the exploration of interactions between microRNAs and transcription factors (TF), in addition to the investigation of associations with diseases, has resulted in the prediction of potential therapeutic drugs. The predictions were validated through the execution of drug-protein molecular docking simulations.
Conclusion
This study provides novel insights into the shared molecular mechanisms between H1N1 infection and GBS. The identification of hub genes, key pathways, and potential therapeutic targets offers a novel direction for targeted therapy in GBS patients infected with H1N1. The findings may contribute to the development of more effective treatment strategies.
