ArticleThe Journal of biological chemistry2012
Proline-proline-glutamic acid (PPE) protein Rv1168c of Mycobacterium tuberculosis augments transcription from HIV-1 long terminal repeat promoter.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 41 citations in OpenAlex.
- Analysis of complete genomes of Mycobacterium tuberculosis sublineage 2.1 (Proto-Beijing) revealed the presence of three pe_pgrs3-pe_pgrs4-like genes.Scientific reports · 2024Article
- Diabetes and tuberculosis: An emerging dual threat to healthcare.World journal of diabetes · 2024Article
- Identification and Phylogenetic Analysis ofTransboundary and emerging diseases · 2023Article
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- The cause-effect relation of tuberculosis on incidence of diabetes mellitus.Frontiers in cellular and infection microbiology · 2023Review
- HIV Latency in Myeloid Cells: Challenges for a Cure.Pathogens (Basel, Switzerland) · 2022Review
- Targeting Cellular and Tissue HIV Reservoirs With Toll-Like Receptor Agonists.Frontiers in immunology · 2019Review
- Dual TLR2 and TLR7 agonists as HIV latency-reversing agents.JCI insight · 2018Article
- PPE17 (Rv1168c) protein of Mycobacterium tuberculosis detects individuals with latent TB infection.PloS one · 2018Article
- The PPE2 protein of Mycobacterium tuberculosis translocates to host nucleus and inhibits nitric oxide production.Scientific reports · 2017Article
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- Reactivation of latent HIV-1 in central memory CD4⁺ T cells through TLR-1/2 stimulation.Retrovirology · 2013Article
- Multifaceted Impact of Host C-C Chemokine CCL2 in the Immuno-Pathogenesis of HIV-1/M. tuberculosis Co-Infection.Frontiers in immunology · 2013Review
- Endocytosis of Mycobacterium tuberculosis heat shock protein 60 is required to induce interleukin-10 production in macrophages.The Journal of biological chemistry · 2013Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells of the monocyte/macrophage lineage are shown to play a role in the pathogenesis of human immunodeficiency virus (HIV). The occurrence of HIV type 1 (HIV-1) infection is found to be accelerated in people infected with Mycobacterium tuberculosis, but the mechanism by which mycobacterial protein(s) induces HIV-1 LTR trans-activation is not clearly understood. We show here that the M. tuberculosis proline-proline-glutamic acid (PPE) protein Rv1168c (PPE17) can augment transcription from HIV-1 LTR in monocyte/macrophage cells. Rv1168c interacts specifically with Toll-like receptor-2 (TLR2) resulting in downstream activation of nuclear factor-κB (NF-κB) resulting in HIV-1 LTR trans-activation. Another PPE protein, Rv1196 (PPE18), was also found to interact with TLR2 but had no effect on HIV-1 LTR trans-activation because of its inability to activate the NF-κB signaling pathway. In silico docking analyses and mutation experiments have revealed that the N-terminal domain of Rv1168c specifically interacts with LRR motifs 15-20 of TLR2, and this site of interaction is different from that of Rv1196 protein (LRR motifs 11-15), indicating that the site of interaction on TLR2 dictates the downstream signaling events leading to activation of NF-κB. This information may help in understanding the mechanism of pathogenesis of HIV-1 during M. tuberculosis co-infection.
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