Latent tuberculosis infection: what we know about its genetic control?

Tuberculosis (Edinb). 2014 Sep;94(5):462-8. doi: 10.1016/j.tube.2014.06.009. Epub 2014 Jul 2.

Abstract

About 90% of all cases of tuberculosis (TB) infection are comprised of latent mycobacterial persistence in the absence of clinical manifestations. In a proportion of latently infected individuals infection eventually reactivates and becomes contagious, seriously influencing epidemiological situation. Mechanisms of Mycobacterium tuberculosis transition to dormancy and TB reactivation are poorly understood, and biological markers of latency remain largely unknown. Data are accumulating that the dynamical equilibrium between the parasite and the host (expressed as a long term asymptomatic infection) and its abrogation (expressed as a reactivation disease) are genetically controlled by both parties. In this short review, the authors summarize the results of experimental studies on genetic regulation of the latent TB infection.

Keywords: Animal models; Gene expression; Host genetics; Latent tuberculosis; Short RNA; Treatment.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antitubercular Agents / therapeutic use
  • Disease Models, Animal
  • Gene Expression Regulation
  • Genetic Predisposition to Disease
  • Host-Pathogen Interactions
  • Humans
  • Latent Tuberculosis / drug therapy
  • Latent Tuberculosis / genetics*
  • Latent Tuberculosis / immunology
  • Latent Tuberculosis / microbiology
  • Mycobacterium tuberculosis / drug effects
  • Mycobacterium tuberculosis / immunology
  • Mycobacterium tuberculosis / pathogenicity*
  • Phenotype
  • RNA, Untranslated / genetics
  • RNA, Untranslated / metabolism
  • Treatment Outcome
  • Virulence

Substances

  • Antitubercular Agents
  • RNA, Untranslated