Mycobacterium tuberculosis enhances human immunodeficiency virus-1 replication by transcriptional activation at the long terminal repeat.

Abstract

construct, live M. tuberculosis increased transcription 20-fold in THP-1 cells, and cell wall components stimulated CAT expression to a lesser extent. The nuclear factor-KB enhancer element was responsible for the majority of the increased CAT activity although two upstream nuclear factor-IL6 sites may also contribute to enhanced transcription. Antibodies to TNF-a and IL-1 inhibited the increase in CAT activity of the HIV-1 long terminal repeat by M. tuberculosis from 21-fold to 8-fold. Stimulation of HIV-1 replication by M. tuberculosis may exacerbate dysfunction of the host immune response in dually infected individuals. (J. Clin. Invest. 1995Invest. . 95:2324Invest. -2331

Differentiation of Monocytes to Macrophages Switches theMycobacterium tuberculosisEffect on HIV-1 Replication from Stimulation to Inhibition: Modulation of Interferon Response and CCAAT/Enhancer Binding Protein β Expression

“…Similar to monocytic THP-1 cells, primary adherent blood monocytes increase HIV-1 replication after infection with M. tuberculosis (7,11). We previously observed that M. tuberculosis suppresses HIV-1 replication in THP-1 cells differentiated to a macrophage-like state by treatment with PMA (15).…”

HIV and Tuberculosis: a Deadly Human Syndemic

“…Moreover, levels of HIV have been found to be higher in M. tuberculosis-infected regions of the lungs than in the uninvolved regions of the same patient (274). Several subsequent studies have provided mechanistic insights into this effect of TB.…”

Viable Mycobacterium avium is required for the majority of human immunodeficiency virus-induced upregulation in monocytoid cells

“…Our work, as well as that of others, downplays the role of mycobacteria-induced soluble factors or NF-kBdependent transcriptional activation in upregulating HIV expression (Shattock et al, 1993;, Dezzutti et al, 1999Ghassemi et al, 2000). Other studies, while reporting an enhancement of HIV p24/RT levels accompanied by cytokine secretion or cytokine-mediated NF-kB-dependent transcriptional activation, did not demonstrate fully a link between these events (Zhang et al, 1995;Goletti et al, 1996Goletti et al, , 1998Vanham et al, 1996). Mancino et al (1997) have reported that viable but not heat-killed M. tuberculosis mediated an increase in HIV production in monocyte-derived macrophages, while Dezzutti et al (1999) have shown that heat-killed and viable MAC enhanced the replication of lymphocytotropic HIV-1 strain LAI in CD8-depleted PBMCs to comparable levels.…”