ArticleBlood2010
HIV-1 Vpr up-regulates expression of ligands for the activating NKG2D receptor and promotes NK cell-mediated killing.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 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
115 citing papers in PubMed, 157 citations in OpenAlex.
- Innate Immune Activity Correlates with CD4 T Cell-Associated HIV-1 DNA Decline during Latency-Reversing Treatment with Panobinostat.Journal of virology · 2015Trial
- Long-term depletion of KIR3DL01+ NK cells by adeno-associated viral-vectored antibody delivery alters chronic SIV infection.PLoS pathogens · 2026Article
- CD56bioRxiv : the preprint server for biology · 2026Article
- Ex vivo-expanded allogeneic Vδ2 T cells specifically reduce reservoirs of HIV-1 following latency reversal.JCI insight · 2026Article
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- CXCR6Frontiers in immunology · 2026Article
- NKp30 and NKG2D contribute to natural killer cell-mediated recognition of HIV-infected cells.iScience · 2025Article
- Emerging role of natural killer cells in non-AIDS comorbidities during suppressive antiretroviral therapy.Current opinion in HIV and AIDS · 2025Review
- From natural defenders to therapeutic warriors: NK cells in HIV immunotherapy.Immunotherapy · 2025Review
- Impaired immune reconstitution in HIV infection: the role of CD4Frontiers in immunology · 2025Article
- The effect of COVID-19 and sex differences on natural killer cell cytotoxicity.Frontiers in cellular and infection microbiology · 2025Article
- HIV controllers: hope for a functional cure.Frontiers in immunology · 2025Review
- Review
- Article
- Vpr attenuates antiviral immune responses and is critical for full pathogenicity of SIViScience · 2023Article
- NK cells from Men Who Have Sex with Men at high risk for HIV-1 infection exhibit higher effector capacity.Scientific reports · 2023Article
- Natural killer cells and their exosomes in viral infections and related therapeutic approaches: where are we?Cell communication and signaling : CCS · 2023Review
- Article
- Mapping the interplay between NK cells and HIV: therapeutic implications.Journal of leukocyte biology · 2023Review
- NK cell subsets and dysfunction during viral infection: a new avenue for therapeutics?Frontiers in immunology · 2023Review
55 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
5 authors at 2 institutions in 1 country.
Funding
Abstract
HIV up-regulates cell-surface expression of specific ligands for the activating NKG2D receptor, including ULBP-1, -2, and -3, but not MICA or MICB, in infected cells both in vitro and in vivo. However, the viral factor(s) involved in NKG2D ligand expression still remains undefined. HIV-1 Vpr activates the DNA damage/stress-sensing ATR kinase and promotes G(2) cell-cycle arrest, conditions known to up-regulate NKG2D ligands. We report here that HIV-1 selectively induces cell-surface expression of ULBP-2 in primary CD4(+) T lymphocytes by a process that is Vpr dependent. Importantly, Vpr enhanced the susceptibility of HIV-1-infected cells to NK cell-mediated killing. Strikingly, Vpr alone was sufficient to up-regulate expression of all NKG2D ligands and thus promoted efficient NKG2D-dependent NK cell-mediated killing. Delivery of virion-associated Vpr via defective HIV-1 particles induced analogous biologic effects in noninfected target cells, suggesting that Vpr may act similarly beyond infected cells. All these activities relied on Vpr ability to activate the ATR-mediated DNA damage/stress checkpoint. Overall, these results indicate that Vpr is a key determinant responsible for HIV-1-induced up-regulation of NKG2D ligands and further suggest an immunomodulatory role for Vpr that may not only contribute to HIV-1-induced CD4(+) T-lymphocyte depletion but may also take part in HIV-1-induced NK-cell dysfunction.
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What OpenQuestion holds
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.