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

Abstract

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.