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Survival mechanisms of pathogenic Mycobacterium tuberculosis H 37 Rv
Author(s) -
Meena Laxman S.,
Rajni
Publication year - 2010
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2010.07666.x
Subject(s) - phagosome , mycobacterium tuberculosis , tuberculosis , pathogen , microbiology and biotechnology , biology , mycobacterium , phagolysosome , virology , bacteria , phagocytosis , genetics , medicine , pathology
Mycobacterium tuberculosis H 37 Rv 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 H 37 Rv 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 tryptophan‐aspartate 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 H 37 Rv 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 H 37 Rv that aids in its survival and pathogenicity.