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The already enormous burden caused by  Mycobacterium tuberculosis  and Human Immunodeficiency Virus type 1 (HIV-1) alone is aggravated by co-infection. Despite obvious differences in the rate of evolution comparing these two human pathogens, genetic diversity plays an important role in the success of both. The extreme evolutionary dynamics of HIV-1 is in the basis of a robust capacity to evade immune responses, to generate drug-resistance and to diversify the population-level reservoir of M group viral subtypes. Compared to HIV-1 and other retroviruses,  M. tuberculosis  generates minute levels of genetic diversity within the host. However, emerging whole-genome sequencing data show that the  M. tuberculosis  complex contains at least nine human-adapted phylogenetic lineages. This level of genetic diversity results in differences in  M. tuberculosis  interactions with the host immune system, virulence and drug resistance propensity. In co-infected individuals, HIV-1 and  M. tuberculosis  are likely to co-colonize host cells. However, the evolutionary impact of the interaction between the host, the slowly evolving  M. tuberculosis  bacteria and the HIV-1 viral “mutant cloud” is poorly understood. These evolutionary dynamics, at the cellular niche of monocytes/macrophages, are also discussed and proposed as a relevant future research topic in the context of single-cell sequencing.

Evolutionary Genetics of Mycobacterium Tuberculosis and HIV-1: “The Tortoise and the Hare”