ArticleThe Journal of experimental medicine2013
CD36-specific antibodies block release of HIV-1 from infected primary macrophages and its transmission to T cells.
Article in The Journal of experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Distinct roles of dopamine receptors in HIV latency reversal in a myeloid cell model.Frontiers in immunology · 2026Article
- CD4+ T cells facilitate replication of primary HIV-1 strains in macrophages and formation of macrophage internal virus-containing compartments.Journal of virology · 2025Article
- The CLIC/GEEC pathway regulates particle uptake and formation of the virus-containing compartment (VCC) in HIV-1-infected macrophages.PLoS pathogens · 2025Article
- Article
- Targeting monocytic Occludin impairs transendothelial migration and HIV neuroinvasion.EMBO reports · 2024Article
- Hidden features: CD36/SR-B2, a master regulator of macrophage phenotype/function through metabolism.Frontiers in immunology · 2024Review
- The function of CD36 inFrontiers in immunology · 2024Review
- Plasma extracellular vesicles and cell-free mitochondrial DNA are associated with cognitive dysfunction in treated older adults with HIV.Journal of neurovirology · 2023Article
- Glycan dependent phenotype differences of HIV-1 generated from macrophage versus CD4Frontiers in immunology · 2023Article
- Lipid droplets fuel SARS-CoV-2 replication and production of inflammatory mediators.PLoS pathogens · 2020Article
- Review
- Spatiotemporal dynamic monitoring of fatty acid-receptor interaction on single living cells by multiplexed Raman imaging.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- HIV-2-Infected Macrophages Produce and Accumulate Poorly Infectious Viral Particles.Frontiers in microbiology · 2020Article
- Macrophage-derived HIV-1 carries bioactive TGF-beta.Scientific reports · 2019Article
- Constitutive Siglec-1 expression confers susceptibility to HIV-1 infection of human dendritic cell precursors.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- T cell metabolism in chronic viral infection.Clinical and experimental immunology · 2019Review
- Myeloid Cell Interaction with HIV: A Complex Relationship.Frontiers in immunology · 2017Review
- Host Immune Responses in HIV-1 Infection: The Emerging Pathogenic Role of Siglecs and Their Clinical Correlates.Frontiers in immunology · 2017Review
- Molecular Determinants Directing HIV-1 Gag Assembly to Virus-Containing Compartments in Primary Macrophages.Journal of virology · 2016Article
- Cell-Free versus Cell-to-Cell Infection by Human Immunodeficiency Virus Type 1 and Human T-Lymphotropic Virus Type 1: Exploring the Link among Viral Source, Viral Trafficking, and Viral Replication.Journal of virology · 2016Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV-1-infected macrophages likely represent viral reservoirs, as they accumulate newly formed virions in internal virus-containing compartments (VCCs). However, the nature and biogenesis of VCCs remain poorly defined. We show that upon HIV-1 infection of primary human macrophages, Gag is recruited to preexisting compartments containing the scavenger receptor CD36, which then become VCCs. Silencing of CD36 in HIV-1-infected macrophages decreases the amount of virions released. Strikingly, soluble anti-CD36 antibodies, but not the natural ligands of CD36, inhibit release of virions from HIV-1-infected macrophages and the transmission of virus to CD4(+) T cells. The effect of the antibodies is potent, rapid, and induces the retention of virions within VCCs. Ectopic expression of CD36 in HeLa cells renders them susceptible to the inhibitory effect of the anti-CD36 mAb upon HIV-1 infection. We show that the anti-CD36 mAb inhibits HIV-1 release by clustering newly formed virions at their site of budding, and that signaling via CD36 is not required. Thus, HIV-1 reservoirs in macrophages may be tackled therapeutically using anti-CD36 antibodies to prevent viral dissemination.
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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.