ArticleInternational journal of molecular sciences2020
HIV-1 Tat Protein Enters Dysfunctional Endothelial Cells via Integrins and Renders Them Permissive to Virus Replication.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- HIV and cardiovascular diseases: a systematic review and comparative risk assessment study.BMJ global health · 2026Pooled it
- Variation in HIV-1 Tat and Vpr protein amino acid sequences and its association with vascular health measures in a South African cohort: an exploratory study.Virology journal · 2025Article
- SLC38A9 is directly involved in Tat-induced endolysosome dysfunction and senescence in astrocytes.Life science alliance · 2025Article
- Review
- HIV-Tat and vascular endothelium: implications in the HIV associated brain, heart, and lung complications.Frontiers in immunology · 2025Review
- Innovative nebulization delivery of lipid nanoparticle-encapsulated siRNA: a therapeutic advance for Staphylococcus aureus-induced pneumonia.Journal of translational medicine · 2024Article
- Bioinformatics Insights on Viral Gene Expression Transactivation: From HIV-1 to SARS-CoV-2.International journal of molecular sciences · 2024Article
- Role of HIV-1 Tat Protein Interactions with Host Receptors in HIV Infection and Pathogenesis.International journal of molecular sciences · 2024Review
- Heterologous DNA Prime/Protein Boost Immunization Targeting Nef-Tat Fusion Antigen Induces Potent T-cell Activity andCurrent HIV research · 2024Article
- High salt intake and HIV infection on endothelial glycocalyx shedding in salt-sensitive hypertension.Frontiers in cell and developmental biology · 2024Review
- HIV gp120/Tat protein-induced epithelial-mesenchymal transition promotes the progression of cervical lesions.AIDS research and therapy · 2023Article
- Recent Advances of Cell-Penetrating Peptides and Their Application as Vectors for Delivery of Peptide and Protein-Based Cargo Molecules.Pharmaceutics · 2023Review
- Cardiovascular Disease and Thrombosis in HIV Infection.Arteriosclerosis, thrombosis, and vascular biology · 2023Review
- Sepsis - it is all about the platelets.Frontiers in immunology · 2023Review
- Kaposi's Sarcoma Lesion Progression in BKV-Tat Transgenic Mice Is Increased by Inflammatory Cytokines and Blocked by Treatment with Anti-Tat Antibodies.International journal of molecular sciences · 2022Article
- HIV-1 Tat and Heparan Sulfate Proteoglycans Orchestrate the Setup ofMolecules (Basel, Switzerland) · 2021Article
- New insights into pathogenesis point to HIV-1 Tat as a key vaccine target.Archives of virology · 2021Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Previous work has shown that the Tat protein of Human Immunodeficiency Virus (HIV)-1 is released by acutely infected cells in a biologically active form and enters dendritic cells upon the binding of its arginine-glycine-aspartic acid (RGD) domain to the α5β1, αvβ3, and αvβ5 integrins. The up-regulation/activation of these integrins occurs in endothelial cells exposed to inflammatory cytokines that are increased in HIV-infected individuals, leading to endothelial cell dysfunction. Here, we show that inflammatory cytokine-activated endothelial cells selectively bind and rapidly take up nano-micromolar concentrations of Tat, as determined by flow cytometry. Protein oxidation and low temperatures reduce Tat entry, suggesting a conformation- and energy-dependent process. Consistently, Tat entry is competed out by RGD-Tat peptides or integrin natural ligands, and it is blocked by anti-α5β1, -αvβ3, and -αvβ5 antibodies. Moreover, modelling-docking calculations identify a low-energy Tat-αvβ3 integrin complex in which Tat makes contacts with both the αv and β3 chains. It is noteworthy that internalized Tat induces HIV replication in inflammatory cytokine-treated, but not untreated, endothelial cells. Thus, endothelial cell dysfunction driven by inflammatory cytokines renders the vascular system a target of Tat, which makes endothelial cells permissive to HIV replication, adding a further layer of complexity to functionally cure and/or eradicate HIV infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.