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Mycobacterium tuberculosisH37Rv is a highly successful pathogen and its success fully relies on its ability to utilize macrophages for its replication and, more importantly, the macrophage should remain viable to host the Mycobacterium. | REVIEW ARTICLE Survival mechanisms of pathogenic Mycobacterium tuberculosis H37Rv Laxman S. Meena and Rajni Institute of Genomics and Integrative Biology Delhi India Keywords dormancy host cell lysosome Mycobacterium phagosome signaling transduction tuberculosis virulence factor Correspondence L. S. Meena Institute of Genomics and Integrative Biology MallRoad Delhi-110007 India Fax 91 11 27667471 Tel 91 11 27666156 E-mail meena@igib.res.in laxmansm72@yahoo.com Received 2 February 2010 revised 12 March 2010 accepted 29 March 2010 doi 10.1111 j.1742-4658.2010.07666.x Mycobacterium tuberculosis H37Rv is a highly successful pathogen and its success fully relies on its ability to utilize macrophages for its replication and more importantly the macrophage should remain viable to host the Mycobacterium. Despite the fact that these phagocytes are usually very effective in internalizing and clearing most of the bacteria M. tuberculosis H37Rv has evolved a number of very effective survival strategies including a the inhibition of phagosome-lysosome fusion b the inhibition of phagosome acidification c the recruitment and retention of tryptophanaspartate containing coat protein on phagosomes to prevent their delivery to lysosomes and d the expression of members of the host-induced repetitive glycine-rich protein family of proteins. However the mechanisms by which M. tuberculosis H37Rv enters the host cell circumvents host defenses and spreads to neighboring cell are not completely understood. Therefore a better understanding of host-pathogen interaction is essential if the global tuberculosis pandemic is ever to be controlled. This review addresses some of the pathogenic strategies of the M. tuberculosis H37Rv that aids in its survival and pathogenicity. Introduction Five decades of tuberculosis TB control programs using potentially efficacious drugs have failed to reduce prevalence of infection by the causative organism Mycobacterium tuberculosis in most parts of the world 1
