AI Article Synopsis

  • - The study investigates how HIV infection affects the immune response to Mycobacterium tuberculosis (M. tuberculosis), particularly focusing on T helper 1 (Th1) cells, in both HIV-negative and chronically HIV-infected individuals in Tanzania.
  • - Results show that chronic HIV infection leads to a significant decrease in M. tuberculosis-specific Th1 cells in asymptomatic individuals, while those with active TB do not show this decline.
  • - Acute HIV infection causes a quick drop in M. tuberculosis-specific Th1 cells in previously TB-asymptomatic individuals, hinting at a link between this depletion and the early development of TB in people with latent M. tuberculosis upon acquiring HIV.

Article Abstract

Background: The acid-fast bacillus Mycobacterium tuberculosis is often the first manifestation of acquired immunodeficiency syndrome in patients infected with human immunodeficiency virus (HIV). This study was conducted to better understand the mechanism underlying M. tuberculosis-specific pathogenicity early after onset of HIV infection.

Methods: M. tuberculosis-specific T helper 1 (Th1) cells were studied in HIV negative (n=114) and chronically HIV infected (n=68) Tanzanian subjects by using early secreted antigenic target 6 (ESAT6) protein or tuberculin (purified protein derivative) with interferon-gamma ELISPOT and intracellular cytokine staining. In a longitudinal study, the effect of acute HIV infection on M. tuberculosis-specific Th1 cells was determined by polychromatic flow cytometric analysis in 5 subjects with latent M. tuberculosis infection who became infected with HIV.

Results: In tuberculosis (TB)-asymptomatic subjects (i.e., subjects with unknown TB status who did not show clinical signs suggestive of TB), chronic HIV infection was associated with a decreased percentage of subjects with detectable M. tuberculosis-specific Th1 cells (P< .001) a decrease which was not observed among subjects with active TB. Acute HIV infection induced a rapid depletion of M. tuberculosis-specific Th1 cells in 4 subjects remained TB asymptomatic, whereas the population of these cells remained stable in subjects who remained HIV negative (P< .01).

Conclusions: Taken together, these data suggest a mechanism of rapid M. tuberculosis-specific Th1 cell depletion that may contribute to the early onset of TB in individuals with latent M. tuberculosis infection who become HIV infected.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650495PMC
http://dx.doi.org/10.1086/593017DOI Listing

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