Abstract
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.
Highlights
Tuberculosis (TB), a disease caused by Mycobacterium tuberculosis infection, is one of the top ten leading causes of death worldwide [1,2]
We describe the genetic diversity and evolution of M. tuberculosis and Human Immunodeficiency Virus type 1 (HIV-1), with particular emphasis on its biomedical implication and impact in host–pathogen interactions
We propose the evolutionary dynamics of the interaction between the host, M. tuberculosis and Human ImmunodeficiencyVirus (HIV)-1, at the cellular niche of monocytes/macrophages, as a future research challenge to the field
Summary
Tuberculosis (TB), a disease caused by Mycobacterium tuberculosis infection, is one of the top ten leading causes of death worldwide [1,2]. “specialist” sublineages presented lower levels of sequence diversity in experimentally validated T cell epitopes [23], indicating a possible role for human adaptive immune system in the definition of host-pathogen combinations that can more likely result in active TB after infection [23]. Other elaborated approaches have been uncovering relevant CD4+ T cell epitopes, including some that are highly prevalent in certain MTBC lineages [62,63,64] Another important feature of the immune response in TB is the balance between pathogen clearance and immunopathology [8,10]. Immune findings highlight the need for an integrative approach to diagnose and treat TB, taking into account important comorbidities such as the ones caused by HIV-1
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