Survival mechanisms of pathogenic Mycobacterium tuberculosis H37Rv.
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.
Meena
Laxman S
LS
Institute of Genomics and Integrative Biology, Delhi, India. meena@igib.res.in
Rajni
D001426:Bacterial Proteins / Q000235:genetics; D002470:Cell Survival; D015964:Gene Expression Regulation, Bacterial; D054884:Host-Pathogen Interactions; D006801:Humans; D008247:Lysosomes / Q000382:microbiology / Q000502:physiology; D008264:Macrophages / Q000382:microbiology; D009169:Mycobacterium tuberculosis / Q000166:cytology / Q000235:genetics / Q000472:pathogenicity*; D010587:Phagocytosis; D010588:Phagosomes / Q000382:microbiology / Q000502:physiology; D011956:Receptors, Cell Surface / Q000502:physiology; D014376:Tuberculosis / Q000382:microbiology; D014774:Virulence
D001426:Bacterial Proteins; D011956:Receptors, Cell Surface