Mechanisms of reactivation of latent tuberculosis infection due to SIV coinfection

J Clin Invest. 2019 Dec 2;129(12):5254-5260. doi: 10.1172/JCI125810.

Abstract

HIV is a major driver of tuberculosis (TB) reactivation. Depletion of CD4+ T cells is assumed to be the basis behind TB reactivation in individuals with latent tuberculosis infection (LTBI) coinfected with HIV. Nonhuman primates (NHPs) coinfected with a mutant simian immunodeficiency virus (SIVΔGY) that does not cause depletion of tissue CD4+ T cells during infection failed to reactivate TB. To investigate the contribution of CD4+ T cell depletion relative to other mechanisms of SIV-induced reactivation of LTBI, we used CD4R1 antibody to deplete CD4+ T cells in animals with LTBI without lentiviral infection. The mere depletion of CD4+ T cells during LTBI was insufficient in generating reactivation of LTBI. Instead, direct cytopathic effects of SIV resulting in chronic immune activation, along with the altered effector T cell phenotypes and dysregulated T cell homeostasis, were likely mediators of reactivation of LTBI. These results revealed important implications for TB control in HIV-coinfected individuals.

Keywords: AIDS/HIV; Infectious disease; T cells; Tuberculosis.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / microbiology
  • CD4-Positive T-Lymphocytes / virology
  • Coinfection / microbiology*
  • Coinfection / virology*
  • Homeostasis
  • Latent Tuberculosis / complications*
  • Latent Tuberculosis / virology
  • Lentivirus
  • Lymphocyte Depletion
  • Macaca mulatta
  • Mutation
  • Mycobacterium tuberculosis
  • Phenotype
  • Simian Acquired Immunodeficiency Syndrome / complications*
  • Simian Acquired Immunodeficiency Syndrome / microbiology
  • Simian Immunodeficiency Virus