Integrative analysis of Poly(A)-seq and RNA-seq reveals transcriptional regulation of poly(A) tail length in tuberculosis

Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a global health challenge, with granulomas-its defining histopathological feature-playing a crucial role in the host's defense and patient outcomes. While poly(A) tail processing, a critical post-transcriptional regulator of RNA lifecycle events, has been studied in diseases like repeat expansion disorders, its role in TB pathogenesis remains unexplored. This study is the first to integrate Poly(A)-seq and RNA-seq to investigate the significance of poly(A) tail length regulation in tuberculosis granulomas. Our findings provide new insights into Mtb pathogenesis and the human immune response, and offer promising avenues for developing targeted host-directed therapeutic strategies.