Investigation of the relationship between chronic hepatitis B and tuberculosis using bioinformatics and systems biology approaches.

Background: Hepatitis B virus (HBV) is a globally prevalent pathogen that poses significant public health challenges. Active HBV replication can trigger immune responses that result in liver damage. Tuberculosis (TB), caused by Methods: To elucidate the relationship between HBV and TB, we performed an integrated bioinformatics analysis using expression profiling and RNA sequencing data from the GSE83148 and GSE126614 datasets. We identified differentially expressed genes (DEGs) associated with both diseases and analyzed shared biological pathways, key genes, transcriptional regulatory networks, and gene-disease associations. Furthermore, we predicted potential therapeutic agents targeting these shared molecular features. Results: A total of 35 overlapping DEGs were identified for in-depth analysis. Functional enrichment revealed that these genes are involved in both immune-related pathways and cellular metabolic regulation, underscoring their potential role in the progression of HBV and TB. Protein-protein interaction (PPI) network analysis highlighted four hub genes: CCL2, CD69, EGR2, and CCL20. Additionally, 35 transcription factors (TFs) were predicted to regulate these hub genes. Several candidate drugs, including etoposide, 8-azaguanine, menaquinone, emetine and N-acetyl-L-cysteine, were identified as potential therapeutic options. The DEGs were also significantly associated with other conditions such as pneumonia. Conclusion: This study provides novel insights into the relationship between HBV and TB, offering potential targets for diagnosis and treatment. Our findings may contribute to the development of integrated strategies to manage HBV infection and TB more effectively.