By Sebastien Gagneux (auth.), Jean Pieters, John D. McKinney (eds.)
Mycobacterium tuberculosis is without doubt one of the so much infamous pathogens on the earth, inflicting the dying of roughly 1.5 million humans every year. an immense challenge within the struggle opposed to tuberculosis is the emergence of lines that experience received resistance to all to be had antibiotics. One key to the luck of M. tuberculosis as a pathogen is its skill to avoid host immune responses at diverse degrees. this isn't just a results of the targeted make-up of M. tuberculosis when it comes to genetic variety and DNA metabolism and its ownership of specialised secretion platforms, but in addition of its skill to hijack the host’s innate immune defence mechanisms.
In this quantity, researchers from various disciplines offer a topical evaluate of the varied mechanisms that give a contribution to the virulence of M. tuberculosis, starting from their genetic, metabolic and molecular make-up, in addition to the complicated options those micro organism make the most of to flee immune destruction inside contaminated hosts.
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Extra resources for Pathogenesis of Mycobacterium tuberculosis and its Interaction with the Host Organism
Mol Biol Evol 23:1129–1135 Sandegren L, Groenheit R, Koivula T, Ghebremichael S, Advani A, Castro E, Pennhag A, Hoffner S, Mazurek J, Pawlowski A, Kan B, Bruchfeld J, Melefors O, Kallenius G (2011) Genomic Stability over 9 Years of an isoniazid resistant Mycobacterium tuberculosis outbreak strain in Sweden. PLoS One 6:e16647 Sandgren A, Strong M, Muthukrishnan P, Weiner BK, Church GM, Murray MB (2009) Tuberculosis drug resistance mutation database. PLoS Med 6:e2 Saunders NJ, Trivedi UH, Thomson ML, Doig C, Laurenson IF, Blaxter ML (2011) Deep resequencing of serial sputum isolates of Mycobacterium tuberculosis during therapeutic failure due to poor compliance reveals stepwise mutation of key resistance genes on an otherwise stable genetic background.
Tuberculosis. Therefore, it was originally assumed that all specialist bypass function in M. tuberculosis would depend on the two canonical Pol IV polymerase homologs, originally annotated as DinP and DinX (Mizrahi and Andersen 1998). The DNA damage response in M. tuberculosis is unusual (Rand et al. 2003) in that it comprises both a classic RecAdependent SOS regulon (Smollett et al. 2012) as well an alternate, RecA-independent, damage regulon (Gamulin et al. 2004) that is controlled by a mycobacterial ClpR-like regulator (Wang et al.
Tuberculosis strains deficient in specific DNA damage repair or reversal components have proved very useful in inferring the nature and extent of genotoxicity of the in vivo environment. These derive in particular from screens of pools of transposon mutants by Transposon Site Hybridization (TraSH) (Sassetti and Rubin 2003) or Designer Arrays for Defined Mutant Analysis (DeADMAn) methodology (Dutta et al. 2010), both of which have elucidated mutants that are comparatively disadvantaged for growth and/or survival as a result of impaired DNA repair or reversal function.
Pathogenesis of Mycobacterium tuberculosis and its Interaction with the Host Organism by Sebastien Gagneux (auth.), Jean Pieters, John D. McKinney (eds.)