ArticlePLoS pathogens2015
Vpr Promotes Macrophage-Dependent HIV-1 Infection of CD4+ T Lymphocytes.
Article in PLoS pathogens, 2015. 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 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.
- Recurrent Severe Subclinical Mastitis and the Risk of HIV Transmission Through Breastfeeding.Frontiers in immunology · 2022Trial
- Self-Dimerization Induced Proximity Targeting Chimeras (SDIPTAC) Lead to DCAF1 Loss of Function and Inhibition of HIV Replication.Journal of medicinal chemistry · 2026Article
- Enhancing antiretroviral delivery to secondary lymph nodes by targeting CD169 + macrophages with HIV-mimicking nanoparticles.Scientific reports · 2025Article
- Targeting HIV myeloid and central nervous system reservoirs for HIV cure.Current opinion in HIV and AIDS · 2025Review
- CRL4-DCAF1 Ubiquitin Ligase Dependent Functions of HIV Viral Protein R and Viral Protein X.Viruses · 2024Review
- Review
- HIV-1 Vpr combats the PU.1-driven antiviral response in primary human macrophages.Nature communications · 2024Article
- Article
- Article
- HIV reprograms host mNature communications · 2021Article
- HIV-infected macrophages resist efficient NK cell-mediated killing while preserving inflammatory cytokine responses.Cell host & microbe · 2021Article
- Review
- Article
- Review
- Review
- Article
- Illuminating the Role of Vpr in HIV Infection of Myeloid Cells.Frontiers in immunology · 2019Review
- Vpr Targets TET2 for Degradation by CRL4Molecular cell · 2018Article
- Resistance of HIV-infected macrophages to CD8Nature immunology · 2018Article
- Dual role of the chromatin-binding factor PHF13 in the pre- and post-integration phases of HIV-1 replication.Open biology · 2017Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Vpr is a conserved primate lentiviral protein that promotes infection of T lymphocytes in vivo by an unknown mechanism. Here we demonstrate that Vpr and its cellular co-factor, DCAF1, are necessary for efficient cell-to-cell spread of HIV-1 from macrophages to CD4+ T lymphocytes when there is inadequate cell-free virus to support direct T lymphocyte infection. Remarkably, Vpr functioned to counteract a macrophage-specific intrinsic antiviral pathway that targeted Env-containing virions to LAMP1+ lysosomal compartments. This restriction of Env also impaired virological synapses formed through interactions between HIV-1 Env on infected macrophages and CD4 on T lymphocytes. Treatment of infected macrophages with exogenous interferon-alpha induced virion degradation and blocked synapse formation, overcoming the effects of Vpr. These results provide a mechanism that helps explain the in vivo requirement for Vpr and suggests that a macrophage-dependent stage of HIV-1 infection drives the evolutionary conservation of Vpr.
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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.