Abstract

Two strains of Mycobacterium tuberculosis complex can be separated as much as 2500 single nucleotide differences (Coscolla and Gagneux, 2014). In that limited amount of diversity, we find an astonishing range of clinical, epidemiological and biological phenotypes. The most striking is the strong host preferences depending on the infecting strain while more subtle differences can be found looking at different human tuberculosis isolates. Those subtle differences are the most difficult to spot given that analysis methods for so little diversity are limited and phenotypes like virulence are difficult to define and measure. Recent genomics advances allow to study the pathogen diversity at a resolution not available before from comparative species level, to global diversity to transmission in local settings. Here, we will review some of these recent results to highlight how population genomics approaches can aid not only to understand how MTBC evolved but also to identify relevant biomedical targets.

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