[Mycobacterium tuberculosis virulence factors and its immune evasion mechanisms]

One-third of the world population is infected with Mycobacterium tuberculosis. When tuberculosis develops, the disease localization, severity, and outcome are highly variable between different individuals. The various manifestations of infection with M. tuberculosis reflect the balance between the bacilli and host defense mechanisms, in which the quality of host defense determines the outcome. Recent studies have identified several mycobacterial cell wall components that may be involved in the key steps of pathogenicity. M. tuberculosis is successful as a pathogen because of its ability to persist in an immunocompetent host. This bacterium lives within the macrophages. Hosts infected with M. tuberculosis mount a strong immune response. This response is usually sufficient to prevent progression to active disease. The strong immune response can control, but not eliminate the bacilli, indicating that M. tuberculosis has evolved mechanisms to modulate or avoid detection by the host immune response. Recent advances have improved our understanding of how M. tuberculosis evades two major antimicrobial mechanisms of macrophages; phagolysosome fusion and the production of toxic reactive nitrogen intermediates (RNI). In this review, the recent evidence of M. tuberculosis evasion from phagolysosome fusion and RNI toxicity, as well as prevention of the recognition of infected macrophages by CD4+ T lymphocytes by inhibiting MHC class II presentation, were discussed.