Induction of HIV type 1 expression correlates with T cell responsiveness to mycobacteria in patients coinfected with HIV type 1 and Mycobacterium tuberculosis

AIDS Res Hum Retroviruses. 2009 Feb;25(2):213-6. doi: 10.1089/aid.2008.0182.

Abstract

An in vitro mononuclear cell system to model the microenvironment of coinfection with HIV-1 and Mycobacterium tuberculosis (MTB) was developed. This cellular system was used to assess the interaction of MTB-infected monocytes and T cells from dually infected HIV-1/TB patients with pulmonary tuberculosis (TB). Subjects with higher induction of HIV-1 gag/pol mRNA expression after MTB stimulation had increased MTB-specific T cell IFN-gamma and TNF-alpha production. Lack of HIV-1 mRNA induction did not correlate with increased induction of regulatory T cells (T-reg) as measured by MTB-induced Foxp3 mRNA. HIV-1 induction did not significantly correlate with clinical parameters including plasma HIV-1 viral load or CD4(+) T cell count. These data model MTB-induced HIV-1 replication at the microenvironment of MTB reactivation/infection. The data suggest that the magnitude of MTB-specific T cell responses drives local viral pathogenesis regardless of the stage of HIV-1 disease as reflected by plasma viral load or CD4(+) T cell count.

Publication types

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

MeSH terms

  • Adolescent
  • Adult
  • Animals
  • CD4 Lymphocyte Count
  • Female
  • Forkhead Transcription Factors / analysis
  • HIV Infections / complications*
  • HIV Infections / immunology*
  • HIV Infections / virology
  • HIV-1 / isolation & purification*
  • Humans
  • Interferon-gamma / biosynthesis
  • Male
  • Middle Aged
  • Mycobacterium tuberculosis / isolation & purification*
  • T-Lymphocyte Subsets / chemistry
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocytes / chemistry
  • T-Lymphocytes / immunology*
  • Tuberculosis, Pulmonary / immunology*
  • Tuberculosis, Pulmonary / microbiology
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Viral Load
  • Young Adult

Substances

  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma