ArticleJournal of virology2018
Semen Exosomes Promote Transcriptional Silencing of HIV-1 by Disrupting NF-κB/Sp1/Tat Circuitry.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 60 citations in OpenAlex.
- Extracellular condensates (ECs) are endogenous modulators of HIV transcription and latency reactivation.Molecular psychiatry · 2026Article
- Plant Lipid Droplets and Derived Lipidic Nano-Assemblies: Structure, Biogenesis and Pharmaceutical Applications.Plant biotechnology journal · 2026Review
- Extracellular vesicles in viral disease management.Current research in microbial sciences · 2026Review
- Bio fluid exosomes: promises, challenges, and future directions in translational medicine.Journal of translational medicine · 2025Review
- Identification of proteins in semen-derived extracellular vesicles that bind to Tat and NF-κB and that may impair HIV replication.Science signaling · 2025Article
- "Silent messengers of chaos: unveiling the dual threat of immune infiltrates in Japanese encephalitis virus neuroinflammatory storm".Virology journal · 2025Review
- Rigorous Process for Isolation of Gut-Derived Extracellular Vesicles (EVs) and the Effect on Latent HIV.Cells · 2025Article
- Innate Antiviral Defense of the Male Reproductive System.Advances in experimental medicine and biology · 2025Review
- Berberine: A dual anti-HIV and anti- cervical cancer compound.Research square · 2024Article
- From stem cells to extracellular vesicles: a new horizon in tissue engineering and regenerative medicine.Cytotechnology · 2024Review
- Extracellular vesicles and endothelial dysfunction in infectious diseases.Journal of extracellular biology · 2024Review
- Unraveling the Connection: Extracellular Vesicles and Non-Small Cell Lung Cancer.International journal of nanomedicine · 2024Review
- Harnessing crosstalk between extracellular vesicles and viruses for disease diagnostics and therapeutics.Extracellular vesicles and circulating nucleic acids · 2024Review
- Biological function of Extracellular Vesicles (EVs): a review of the field.Molecular biology reports · 2023Review
- Article
- DDX3 suppresses hepatocellular carcinoma progression through modulating the secretion and composition of exosome.American journal of cancer research · 2023Article
- Exosome and virus infection.Frontiers in immunology · 2023Review
- Blood plasma derived extracellular vesicles (BEVs): particle purification liquid chromatography (PPLC) and proteomic analysis reveals BEVs as a potential minimally invasive tool for predicting response to breast cancer treatment.Breast cancer research and treatment · 2022Article
- Chronic delta-9-tetrahydrocannabinol (THC) treatment counteracts SIV-induced modulation of proinflammatory microRNA cargo in basal ganglia-derived extracellular vesicles.Journal of neuroinflammation · 2022Article
- Extracellular vesicles and lipoproteins - Smart messengers of blood cells in the circulation.Journal of extracellular biology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Exosomes play various roles in host responses to cancer and infective agents, and semen exosomes (SE) inhibit HIV-1 infection and transmission, although the mechanism(s) by which this occurs is unclear. Here, we show that SE block HIV-1 proviral transcription at multiple transcriptional checkpoints, including transcription factor recruitment to the long terminal repeat (LTR), transcription initiation, and elongation. Biochemical and functional studies show that SE inhibit HIV-1 LTR-driven viral gene expression and virus replication. Through partitioning of the HIV-1 RNA, we found that SE reduced the optimal expression of various viral RNA species. Chromatin immunoprecipitation-real-time quantitative PCR (ChIP-RT-qPCR) and electrophoretic mobility shift assay (EMSA) analysis of infected cells identified the human transcription factors NF-κB and Sp1, as well as RNA polymerase (Pol) II and the viral protein transcriptional activator (Tat), as targets of SE. Of interest, SE inhibited HIV-1 LTR activation mediated by HIV-1 or Tat, but not by the mitogen phorbol myristate acetate (PMA) or tumor necrosis factor alpha (TNF-α). SE inhibited the DNA binding activities of NF-κB and Sp1 and blocked the recruitment of these transcription factors and Pol II to the HIV-1 LTR promoter. Importantly, SE directly blocked NF-κB, Sp1, and Pol II binding to the LTR and inhibited the interactions of Tat/NF-κB and Tat/Sp1, suggesting that SE-mediated inhibition of the functional quadripartite complex NF-κB-Sp1-Pol II-Tat may be a novel mechanism of proviral transcription repression. These data provide a novel molecular basis for SE-mediated inhibition of HIV-1 and identify Tat as a potential target of SE.
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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 OpenQuestion graph.