TUBERCULOSIS: MECHANISMS OF PATHOGENESIS OF MYCOBACTERIUM TUBERCULOSIS

Abstract

Tuberculosis continues to be a major global public health challenge. Mycobacterium tuberculosis, the etiological agent of the disease, has sophisticated pathogenic mechanisms that allow it to invade, survive and replicate in the host. In addition, Mtb uses several mechanisms to evade the host immune response, such as inhibition of phagosome-lysosome fusion, modulation of macrophage function and induction of granulomas, environments that favor latency of the infection. The interaction between Mtb and the host immune system is complex, involving immune cells, such as macrophages, T lymphocytes and epithelial cells, with Mtb manipulating these responses to ensure its survival. The increasing resistance of Mtb to traditional drugs and the difficulties in treating resistant forms of the disease make research into new treatments more urgent. In this sense, the identification of molecular biomarkers, such as Mtb messenger RNA, and the exploration of key protein inhibitors, such as Antigen 85C, present promising approaches for the development of more effective therapies. This literature review addresses the main microbiological aspects related to the pathogenesis of M. tuberculosis, highlighting its cellular structure, virulence factors and interactions with the host immune system.