ArticlePloS one2017
HIV-Tat regulates macrophage gene expression in the context of neuroAIDS.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Resistance Training Improves Cognitive Function and Depression Without Changing BDNF Levels in People Living with HIV: a Randomized Controlled Clinical Trial.AIDS and behavior · 2025Trial
- Neuroinflammatory crosstalk between microglia and astrocytes increases viral replication in an iPSC-derived model of CNS HIV infection.Scientific reports · 2026Article
- Neuroinflammatory crosstalk between microglia and astrocytes increases viral replication in an iPSC-derived model of CNS HIV infection.bioRxiv : the preprint server for biology · 2025Article
- Compensatory reactions of B cells in response to chronic HIV-1 Tat exposure.Journal of cellular physiology · 2025Article
- Intracellular HIV-1 Tat regulator induces epigenetic changes in the DNA methylation landscape.Frontiers in immunology · 2025Article
- Review
- BDNF and NGF Expression in Preneoplastic Cervical Disease According to HIV Status.International journal of molecular sciences · 2023Article
- HIV-1 Transcriptional Activator Tat InhibitsBiomolecules · 2023Article
- Article
- Intact HIV Proviruses Persist in the Brain Despite Viral Suppression with ART.Annals of neurology · 2022Article
- Neuropathogenesis of HIV-1: insights from across the spectrum of acute through long-term treated infection.Seminars in immunopathology · 2022Review
- Integrated Analysis of the miRNA-mRNA Regulatory Network Involved in HIV-Associated Neurocognitive Disorder.Pathogens (Basel, Switzerland) · 2022Article
- Article
- HIV-1 Transactivator of Transcription (Tat) Co-operates With AP-1 Factors to EnhanceFrontiers in cell and developmental biology · 2021Article
- Functional impact of HIV-1 Tat on cells of the CNS and its role in HAND.Cellular and molecular life sciences : CMLS · 2020Review
- The Role of Brain Derived Neurotrophic Factor in HIV-Associated Neurocognitive Disorder: From the Bench-Top to the Bedside.Neuropsychiatric disease and treatment · 2020Review
- Peroxisome Proliferator-Activated Receptor-gamma agonists exhibit anti-inflammatory and antiviral effects in an EcoHIV mouse model.Scientific reports · 2019Article
- Genetic variation and function of the HIV-1 Tat protein.Medical microbiology and immunology · 2019Review
- Sirtuin 1-Chromatin-Binding Dynamics Points to a Common Mechanism Regulating Inflammatory Targets in SIV Infection and in the Aging Brain.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018Article
- The role of human dopamine transporter in NeuroAIDS.Pharmacology & therapeutics · 2018Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Despite the success of cART, greater than 50% of HIV infected people develop cognitive and motor deficits termed HIV-associated neurocognitive disorders (HAND). Macrophages are the major cell type infected in the CNS. Unlike for T cells, the virus does not kill macrophages and these long-lived cells may become HIV reservoirs in the brain. They produce cytokines/chemokines and viral proteins that promote inflammation and neuronal damage, playing a key role in HIV neuropathogenesis. HIV Tat is the transactivator of transcription that is essential for replication and transcriptional regulation of the virus and is the first protein to be produced after HIV infection. Even with successful cART, Tat is produced by infected cells. In this study we examined the role of the HIV Tat protein in the regulation of gene expression in human macrophages. Using THP-1 cells, a human monocyte/macrophage cell line, and their infection with lentivirus, we generated stable cell lines that express Tat-Flag. We performed ChIP-seq analysis of these cells and found 66 association sites of Tat in promoter or coding regions. Among these are C5, CRLF2/TSLPR, BDNF, and APBA1/Mint1, genes associated with inflammation/damage. We confirmed the association of Tat with these sequences by ChIP assay and expression of these genes in our THP-1 cell lines by qRT-PCR. We found that HIV Tat increased expression of C5, APBA1, and BDNF, and decreased CRLF2. The K50A Tat-mutation dysregulated expression of these genes without affecting the binding of the Tat complex to their gene sequences. Our data suggest that HIV Tat, produced by macrophage HIV reservoirs in the brain despite successful cART, contributes to neuropathogenesis in HIV-infected people.
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Registered trials
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