Exploring the shared pathogenic mechanisms of tuberculosis and COVID-19: emphasizing the role of VNN1 in severe COVID-19.

BACKGROUND

In recent years, COVID-19 and tuberculosis have emerged as major infectious diseases, significantly contributing to global mortality as respiratory illnesses. There is increasing evidence of a reciprocal influence between these diseases, exacerbating their incidence, severity, and mortality rates.

METHODS

This study involved retrieving COVID-19 and tuberculosis data from the GEO database and identifying common differentially expressed genes. Machine learning techniques, specifically random forest analysis, were applied to pinpoint key genes for diagnosing COVID-19. The Cibersort algorithm was employed to estimate immune cell infiltration in individuals with COVID-19. Additionally, single-cell sequencing was used to study the distribution of VNN1 within immune cells, and molecular docking provided insights into potential drugs targeting these critical prognosis genes.

RESULTS

GMNN, SCD, and FUT7 were identified as robust diagnostic markers for COVID-19 across training and validation datasets. Importantly, VNN1 was associated with the progression of severe COVID-19, showing a strong correlation with clinical indicators and immune cell infiltration. Single-cell sequencing demonstrated a predominant distribution of VNN1 in neutrophils, and molecular docking highlighted potential pharmacological targets for VNN1.

CONCLUSIONS

This study enhances our understanding of the shared pathogenic mechanisms underlying tuberculosis and COVID-19, providing essential insights that could improve the diagnosis and treatment of severe COVID-19 cases.