ArticleProceedings of the National Academy of Sciences of the United States of America2019
HIV-1 Vpr counteracts HLTF-mediated restriction of HIV-1 infection in T cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Article
- OICR-41103 as a chemical probe for the DCAF1 WD40 domain.Communications biology · 2025Article
- Article
- HIV-1 Vpr orchestrates ciTRAN upregulation through TGF-β induction.PLoS pathogens · 2025Article
- SIV-specific neutralizing antibody induction following selection of a PI3K drive-attenuatedeLife · 2025Article
- 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
- HIV-1 Vpr Functions in Primary CD4Viruses · 2024Review
- Vpr attenuates antiviral immune responses and is critical for full pathogenicity of SIViScience · 2023Article
- The helicase-like transcription factor redirects the autophagic flux and restricts human T cell leukemia virus type 1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Current and prospective strategies for advancing the targeted delivery of CRISPR/Cas system via extracellular vesicles.Journal of nanobiotechnology · 2023Review
- Article
- Article
- Global post-translational modification profiling of HIV-1-infected cells reveals mechanisms of host cellular pathway remodeling.Cell reports · 2022Article
- CHAF1A/B mediate silencing of unintegrated HIV-1 DNAs early in infection.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Human immunodeficiency virus-1 core: The Trojan horse in virus-host interaction.Frontiers in microbiology · 2022Review
- The HCV Envelope Glycoprotein Down-Modulates NF-κB Signalling and Associates With Stimulation of the Host Endoplasmic Reticulum Stress Pathway.Frontiers in immunology · 2022Article
- Structure of HIV-1 Vpr in complex with the human nucleotide excision repair protein hHR23A.Nature communications · 2021Article
- Huntingtin-Interacting Protein 1 Promotes Vpr-Induced G2 Arrest and HIV-1 Infection in Macrophages.Viruses · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Lentiviruses, including HIV-1, possess the ability to enter the nucleus through nuclear pore complexes and can infect interphase cells, including those actively replicating chromosomal DNA. Viral accessory proteins hijack host cell E3 enzymes to antagonize intrinsic defenses, and thereby provide a more permissive environment for virus replication. The HIV-1 Vpr accessory protein reprograms CRL4
Indexed as
Identifiers
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.