ArticleJournal of virology2014
Exosomes from human immunodeficiency virus type 1 (HIV-1)-infected cells license quiescent CD4+ T lymphocytes to replicate HIV-1 through a Nef- and ADAM17-dependent mechanism.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
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Who cites it
130 citing papers in PubMed, 170 citations in OpenAlex.
- HIV-1 Nef generates lasting innate immune memory in haematopoietic stem and progenitor cells in vivo.EMBO reports · 2026Article
- T cell-inspired therapeutic delivery platforms: From nanomedicines to cell therapy.Materials today. Bio · 2026Review
- Review
- Exosomal nanocarriers of immune fate: molecular insights into cancer immunity, pathogen defense, and emerging immunotherapies.Clinical and experimental immunology · 2026Review
- Exosomes in Cancer Biology: Emerging Biomarkers and Therapeutic Targets.Journal of Cancer · 2026Review
- Astragalus polysaccharide promotes latent HIV-1 reactivation via exosome-mediated modulation of the PI3K/AKT/NF-κB axis.Extracellular vesicles and circulating nucleic acids · 2026Article
- From immune desert to hot tumor: the tripartite synergy of tumor microenvironment-exosomes-immunogenic cell death in pioneering solutions.Frontiers in immunology · 2026Review
- Using common features of viruses and EVs for a novel EV-based lateral flow test for HIV.Extracellular vesicle · 2025Article
- Characterization of HIV-1 Particles Co-Purified With Three Extracellular Vesicle Subtypes From the Raji CD4 DCIR Cell Line, a Hybrid Model of CD4 T Cells and Dendritic Cells.Journal of extracellular biology · 2025Article
- Unveiling the intricacies of exosome biology: from biogenesis to therapeutic applications.Histochemistry and cell biology · 2025Review
- A game of hide-and-seek: how extracellular vesicles evade the immune system.Drug delivery and translational research · 2025Review
- Zika Virus Infection Modulates Extracellular Vesicle Biogenesis and Morphology in Human Umbilical Cord Endothelial Cells: A Proteomic and Microscopic Analysis.Microorganisms · 2025Article
- A Primer on Proteomic Characterization of Intercellular Communication in a Virus Microenvironment.Molecular & cellular proteomics : MCP · 2025Review
- Exosomes at the crossroads of HIV-1 pathogenesis and therapeutics.Frontiers in immunology · 2025Review
- Serum ADAM17 levels pre-antiviral therapy correlate with HIV patient immune reconstitution.Heliyon · 2024Article
- Exosome therapeutics for non-small cell lung cancer tumorigenesis.Cancer cell international · 2024Review
- Exosomes That Have Different Cellular Origins Followed by the Impact They Have on Prostate Tumor Development in the Tumor Microenvironment.Cancer reports (Hoboken, N.J.) · 2024Review
- Therapeutic potential of exosomes derived from mesenchymal stem cells for treatment of systemic lupus erythematosus.Journal of inflammation (London, England) · 2024Review
- The Role of Extracellular Vesicles in Pandemic Viral Infections.Journal of microbiology (Seoul, Korea) · 2024Review
- Extracellular vesicles as tools and targets in therapy for diseases.Signal transduction and targeted therapy · 2024Review
70 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledResting CD4+ T lymphocytes resist human immunodeficiency virus (HIV) infection. Here, we provide evidence that exosomes from HIV-1-infected cells render resting human primary CD4+ T lymphocytes permissive to HIV-1 replication. These results were obtained with transwell cocultures of HIV-1-infected cells with quiescent CD4+ T lymphocytes in the presence of inhibitors of exosome release and were confirmed using exosomes purified from supernatants of HIV-1-infected primary CD4+ T lymphocytes. We found that the expression of HIV-1 Nef in exosome-producing cells is both necessary and sufficient for cell activation as well as HIV-1 replication in target CD4+ T lymphocytes. We also identified a Nef domain important for the effects we observed, i.e., the 62EEEE65 acidic cluster domain. In addition, we observed that ADAM17, i.e., a disintegrin and metalloprotease converting pro-tumor necrosis factor alpha (TNF-α) in its mature form, associates with exosomes from HIV-1-infected cells, and plays a key role in the HIV-1 replication in quiescent CD4+ T lymphocytes. Treatment with an inhibitor of ADAM17 abolished both activation and HIV-1 replication in resting CD4+ T lymphocytes. TNF-α is the downstream effector of ADAM17 since the treatment of resting lymphocytes with anti-TNF-α antibodies blocked the HIV-1 replication. The data presented here are consistent with a model where Nef induces intercellular communication through exosomes to activate bystander quiescent CD4+ T lymphocytes, thus stimulating viral spread. IMPORTANCE: Overall, our findings support the idea that HIV evolved to usurp the exosome-based intercellular communication network to favor its spread in infected hosts.
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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 OpenQuestion graph.