ArticleScientific reports2020
Neutrophil extracellular traps from healthy donors and HIV-1-infected individuals restrict HIV-1 production in macrophages.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Mast cells release DNA Extracellular Traps (DETs) in response to SARS-CoV-2 and its spike protein.Cell communication and signaling : CCS · 2026Article
- Neutrophil extracellular traps promote macrophage activation through Toll-like receptor engagement and PKA and NF-kB signaling pathways.Cell communication and signaling : CCS · 2026Article
- Mucosal Dynamics Contributing to Innate Immune Responses to HIV in the Human Female Genital Tract.Viruses · 2026Review
- Innate Immune Protection Against HIV in the Female Genital Tract.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Review
- Neutrophils in HIV pathogenesis: dual roles, clinical implications, and therapeutic frontiers.Annals of medicine and surgery (2012) · 2025Review
- Pentatrichomonas hominis induces extracellular traps formation of macrophages via the TLR2/NADPH/PAD4 pathway.Parasites & vectors · 2025Article
- Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024Review
- The Diagnostic, Prognostic, and Therapeutic Potential of Cell-Free DNA with a Special Focus on COVID-19 and Other Viral Infections.International journal of molecular sciences · 2023Review
- Low-density granulocytes display immature cells with enhanced NET formation in people living with HIV.Scientific reports · 2023Article
- The State of Art of Extracellular Traps in Protozoan Infections (Review).Frontiers in immunology · 2021Review
- Platelets in HIV: A Guardian of Host Defence or Transient Reservoir of the Virus?Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Neutrophils release extracellular traps (NETs) after interaction with microorganisms and physiological or synthetic products. NETs consist of decondensed chromatin complexed with proteins, some of them with microbicidal properties. Because NETs can modulate the functioning of HIV-1 target cells, we aimed to verify whether they modify HIV-1 replication in macrophages. We found that exposure of HIV-1-infected macrophages to NETs resulted in significant inhibition of viral replication. The NET anti-HIV-1 action was independent of other soluble factors released by the activated neutrophils, but otherwise dependent on the molecular integrity of NETs, since NET-treatment with protease or DNase abolished this effect. NETs induced macrophage production of the anti-HIV-1 β-chemokines Rantes and MIP-1β, and reduced the levels of integrated HIV-1 DNA in the macrophage genome, which may explain the decreased virus production by infected macrophages. Moreover, the residual virions released by NET-treated HIV-1-infected macrophages lost infectivity. In addition, elevated levels of DNA-elastase complexes were detected in the plasma from HIV-1-infected individuals, and neutrophils from these patients released NETs, which also inhibited HIV-1 replication in in vitro infected macrophages. Our results reveal that NETs may function as an innate immunity mechanism able to restrain HIV-1 production in macrophages.
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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.