ArticlePloS one2012
The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Effect of therapeutic intensification followed by HIV DNA prime and rAd5 boost vaccination on HIV-specific immunity and HIV reservoir (EraMune 02): a multicentre randomised clinical trial.The lancet. HIV · 2015Trial
- Promoter DNA methylation of farnesoid X receptor and pregnane X receptor modulates the intrahepatic cholestasis of pregnancy phenotype.PloS one · 2014Trial
- Host restriction factors and p17-Driven inflammaging in HIV-1: From molecular pathogenesis to functional cure.AIMS microbiology · 2026Review
- Hidden features: CD36/SR-B2, a master regulator of macrophage phenotype/function through metabolism.Frontiers in immunology · 2024Review
- The Cardiac Syndecan-2 Interactome.Frontiers in cell and developmental biology · 2020Article
- HIV infection alters the human epigenetic landscape.Gene therapy · 2019Article
- p17 from HIV induces brain endothelial cell angiogenesis through EGFR-1-mediated cell signalling activation.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Article
- The HIV matrix protein p17 induces hepatic lipid accumulation via modulation of nuclear receptor transcriptoma.Scientific reports · 2015Article
- The HIV matrix protein p17 promotes the activation of human hepatic stellate cells through interactions with CXCR2 and Syndecan-2.PloS one · 2014Article
- HIV-1 Nef impairs key functional activities in human macrophages through CD36 downregulation.PloS one · 2014Article
- Ruxolitinib and tofacitinib are potent and selective inhibitors of HIV-1 replication and virus reactivation in vitro.Antimicrobial agents and chemotherapy · 2014Article
- A possible role for CCR5 in the progression of atherosclerosis in HIV-infected patients: a cross-sectional study.AIDS research and therapy · 2013Article
- Synthetic FXR agonist GW4064 prevents diet-induced hepatic steatosis and insulin resistance.Pharmaceutical research · 2013Article
- Type I Interferon at the Interface of Antiviral Immunity and Immune Regulation: The Curious Case of HIV-1.Scientifica · 2013Review
- HIV-1 infection is associated with changes in nuclear receptor transcriptome, pro-inflammatory and lipid profile of monocytes.BMC infectious diseases · 2012Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLong-term remission of HIV-1 disease can be readily achieved by combinations of highly effective antiretroviral therapy (HAART). However, a residual persistent immune activation caused by circulating non infectious particles or viral proteins is observed under HAART and might contribute to an higher risk of non-AIDS pathologies and death in HIV infected persons. A sustained immune activation supports lipid dysmetabolism and increased risk for development of accelerated atehrosclerosis and ischemic complication in virologically suppressed HIV-infected persons receiving HAART.
aimWhile several HIV proteins have been identified and characterized for their ability to maintain immune activation, the role of HIV-p17, a matrix protein involved in the viral replication, is still undefined.
resultsHere, we report that exposure of macrophages to recombinant human p17 induces the expression of proinflammatory and proatherogenic genes (MCP-1, ICAM-1, CD40, CD86 and CD36) while downregulating the expression of nuclear receptors (FXR and PPARγ) that counter-regulate the proinflammatory response and modulate lipid metabolism in these cells. Exposure of macrophage cell lines to p17 activates a signaling pathway mediated by Rack-1/Jak-1/STAT-1 and causes a promoter-dependent regulation of STAT-1 target genes. These effects are abrogated by sera obtained from HIV-infected persons vaccinated with a p17 peptide. Ligands for FXR and PPARγ counteract the effects of p17.
conclusionsThe results of this study show that HIV p17 highjacks a Rack-1/Jak-1/STAT-1 pathway in macrophages, and that the activation of this pathway leads to a simultaneous dysregulation of immune and metabolic functions. The binding of STAT-1 to specific responsive elements in the promoter of PPARγ and FXR and MCP-1 shifts macrophages toward a pro-atherogenetic phenotype characterized by high levels of expression of the scavenger receptor CD36. The present work identifies p17 as a novel target in HIV therapy and grounds the development of anti-p17 small molecules or vaccines.
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