ArticleJournal of virology2006
DC-SIGN and CLEC-2 mediate human immunodeficiency virus type 1 capture by platelets.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
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.
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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.
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Who cites it
130 citing papers in PubMed, 265 citations in OpenAlex.
- Soluble CLEC-2 is generated independently of ADAM10 and is increased in plasma in acute coronary syndrome: comparison with soluble GPVI.International journal of hematology · 2019Trial
- Beyond Hemostasis: Platelets' Multifaceted Functions in Immune Responses.Life (Basel, Switzerland) · 2026Review
- Viral subversion of megakaryopoiesis: reshaping the landscapes of immune regulation.Infection · 2026Review
- Platelet-like particles released from Ebola virus-infected megakaryocytic cells behave like virus-like particles.PLoS pathogens · 2026Article
- Beyond hemostasis, the immunomodulatory nature of platelets.Research and practice in thrombosis and haemostasis · 2025Review
- Article
- Over-activation and dysfunction of platelet-NK cell aggregates in HIV-infected individuals.Journal of translational medicine · 2025Article
- Dengue virus infection: how platelet-leukocyte crosstalk shapes thrombotic events and inflammation.Molecular biology reports · 2025Review
- Platelets in infection: intrinsic roles and functional outcomes.Frontiers in immunology · 2025Review
- Characterization of Platelet Receptors and Their Involvement in Immune Activation of These Cells.International journal of molecular sciences · 2024Review
- Beyond basic characterization and omics: Immunomodulatory roles of platelet-derived extracellular vesicles unveiled by functional testing.Journal of extracellular vesicles · 2024Article
- Article
- Macrophage- and CD4+ T cell-derived SIV differ in glycosylation, infectivity and neutralization sensitivity.PLoS pathogens · 2024Article
- The role of platelets in sepsis: A review.Biomolecules & biomedicine · 2024Review
- Abnormalities in C-type lectin-like receptor 2 in a patient with Gorham-Stout disease: the first case report.Research and practice in thrombosis and haemostasis · 2024Article
- Review
- Inhibition of SARS-CoV-2-mediated thromboinflammation by CLEC2.Fc.EMBO molecular medicine · 2023Article
- Dabie bandavirus infection induces macrophagic pyroptosis and this process is attenuated by platelets.PLoS neglected tropical diseases · 2023Article
- Glycomimetics for the inhibition and modulation of lectins.Chemical Society reviews · 2023Review
- COVID-19 vaccines adverse events: potential molecular mechanisms.Immunologic research · 2023Review
70 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelets can engulf human immunodeficiency virus type 1 (HIV-1), and a significant amount of HIV-1 in the blood of infected individuals is associated with these cells. However, it is unclear how platelets capture HIV-1 and whether platelet-associated virus remains infectious. DC-SIGN and other lectins contribute to capture of HIV-1 by dendritic cells (DCs) and facilitate HIV-1 spread in DC/T-cell cocultures. Here, we show that platelets express both the C-type lectin-like receptor 2 (CLEC-2) and low levels of DC-SIGN. CLEC-2 bound to HIV-1, irrespective of the presence of the viral envelope protein, and facilitated HIV-1 capture by platelets. However, a substantial fraction of the HIV-1 binding activity of platelets was dependent on DC-SIGN. A combination of DC-SIGN and CLEC-2 inhibitors strongly reduced HIV-1 association with platelets, indicating that these lectins are required for efficient HIV-1 binding to platelets. Captured HIV-1 was maintained in an infectious state over several days, suggesting that HIV-1 can escape degradation by platelets and might use these cells to promote its spread. Our results identify CLEC-2 as a novel HIV-1 attachment factor and provide evidence that platelets capture and transfer infectious HIV-1 via DC-SIGN and CLEC-2, thereby possibly facilitating HIV-1 dissemination in infected patients.
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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.