ArticleThe Journal of clinical investigation2016
Macrophages sustain HIV replication in vivo independently of T cells.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 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
170 citing papers in PubMed.
- Vedolizumab and ART in recent HIV-1 infection unveil the role of α4β7 in reservoir size.JCI insight · 2024Trial
- Treatment with integrase inhibitor suggests a new interpretation of HIV RNA decay curves that reveals a subset of cells with slow integration.PLoS pathogens · 2017Trial
- JQKD82 Inhibits HIV Infection of Macrophages Through Blocking Viral Entry and Enhancing Antiviral ISG Responses.Journal of medical virology · 2026Article
- Identification of the cellular factor KLF16 as a novel epigenetic repressor of HIV-1 transcription.Research square · 2026Article
- Identification of the cellular transcription factor KLF16 as a novel repressive epigenetic repressor of HIV-1 transcription.bioRxiv : the preprint server for biology · 2026Article
- Glycolysis inhibition in tuberculosis-driven metabolic rewiring reduces HIV-1 spread in macrophages.Life science alliance · 2026Article
- Review
- The decay of HIV under anti-retroviral therapy is biphasic even in humanized mice with just T cells.Journal of virology · 2026Article
- HIV impairs and exploits pulmonary Th17 and Th22 cell-mediated immune responses to Mycobacterium tuberculosis.PLoS pathogens · 2026Article
- Activation of cytosolic DNA sensing in NCM460 intestinal epithelial cells induces antiviral factors that restrict HIV infection in macrophages.Frontiers in immunology · 2026Article
- HIV-1 Tat protein alters medial prefrontal cortex neuronal activity and recognition memory.iScience · 2025Article
- Monocytes across life span in HIV infection: lights and shadows.Current opinion in HIV and AIDS · 2025Review
- A comprehensive overview on the crosstalk between microRNAs and viral pathogenesis and infection.Medicinal research reviews · 2025Review
- Article
- Immune Alterations and Viral Reservoir Atlas in SIV-Infected Chinese Rhesus Macaques.Infectious disease reports · 2025Review
- Article
- HIV-1 N-myristoylation-dependent hijacking of late endosomes/lysosomes to drive Gag assembly in macrophages.Journal of cell science · 2024Article
- Differences in HIV-1 reservoir size, landscape characteristics and decay dynamics in acute and chronic treated HIV-1 Clade C infection.medRxiv : the preprint server for health sciences · 2024Article
- Targeting monocytic Occludin impairs transendothelial migration and HIV neuroinvasion.EMBO reports · 2024Article
- Review
110 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
13 authors.
Funding
Abstract
Macrophages have long been considered to contribute to HIV infection of the CNS; however, a recent study has contradicted this early work and suggests that myeloid cells are not an in vivo source of virus production. Here, we addressed the role of macrophages in HIV infection by first analyzing monocytes isolated from viremic patients and patients undergoing antiretroviral treatment. We were unable to find viral DNA or viral outgrowth in monocytes isolated from peripheral blood. To determine whether tissue macrophages are productively infected, we used 3 different but complementary humanized mouse models. Two of these models (bone marrow/liver/thymus [BLT] mice and T cell-only mice [ToM]) have been previously described, and the third model was generated by reconstituting immunodeficient mice with human CD34+ hematopoietic stem cells that were devoid of human T cells (myeloid-only mice [MoM]) to specifically evaluate HIV replication in this population. Using MoM, we demonstrated that macrophages can sustain HIV replication in the absence of T cells; HIV-infected macrophages are distributed in various tissues including the brain; replication-competent virus can be rescued ex vivo from infected macrophages; and infected macrophages can establish de novo infection. Together, these results demonstrate that macrophages represent a genuine target for HIV infection in vivo that can sustain and transmit infection.
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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.