**1. Introduction**

292 Understanding Tuberculosis – Deciphering the Secret Life of the Bacilli

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> *Mycobacterium tuberculosis* (*M. tuberculosis*) is the causative agent of tuberculosis disease. According to the Global Tuberculosis Control 2010 report of the World Health Organization http://www.who.int/tb/publications/global\_report/en/, approximately one-third of the world's population is latently infected with *M. tuberculosis* and about two million people die of this disease every year. The emergence of multi- and extensively- drug resistant strains to the currently available drugs makes the development of new therapeutic strategies a priority. However, the mechanisms underlying pathogenesis, virulence and persistence of infections caused by *M. tuberculosis* are not completely understood (Nathan, 2009; Lawn & Zumla, 2011).

> *M. tuberculosis* is one of the most successful human pathogens. It has evolved diverse strategies to ensure growth and survival inside the hostile environment of macrophages, its primary host cells (Ehrt & Schnappinger, 2009; Meena & Rajni, 2010). The molecular mechanisms of *M. tuberculosis* pathogenesis are under active investigation, since they could provide the basis for a rationalized drug design. These include inhibition of phagosome maturation into phagolysosomes (Armstrong & Hart, 1971; MacMicking *et al.*, 2003), inhibition of the acidification of *Mycobacterium-*harboring phagosomes (Sturgill-Koszycki *et al.*, 1994), DNA repair and protein repair or degradation (Boshoff *et al.*, 2003; Gandotra *et al.*, 2007; Lee *et al.*, 2009), as well as decomposition of cytotoxic reactive nitrogen and oxygen species formed upon phagocytosis (Nathan & Shiloh, 2000; Shiloh & Nathan, 2000; Bedard & Krause, 2007). These should be considered as complementary survival mechanisms. Herein, we will focus in the antioxidant systems of *M. tuberculosis*, and particularly, in thioldependent peroxidases.
