ReviewFrontiers in microbiology2014
DNA damage repair machinery and HIV escape from innate immune sensing.
Review in Frontiers in microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
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Who cites it
34 citing papers in PubMed.
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- CRL4-DCAF1 Ubiquitin Ligase Dependent Functions of HIV Viral Protein R and Viral Protein X.Viruses · 2024Review
- Review
- Article
- Vpr attenuates antiviral immune responses and is critical for full pathogenicity of SIViScience · 2023Article
- Inhibition of ATM-directed antiviral responses by HIV-1 Vif.PLoS pathogens · 2023Article
- Article
- Identification of key genes and pathways between mild-moderate and severe asthmatics via bioinformatics analysis.Scientific reports · 2022Article
- Tuning Rex rules HTLV-1 pathogenesis.Frontiers in immunology · 2022Review
- A virus-free cellular model recapitulates several features of severe COVID-19.Scientific reports · 2021Article
- ZBTB2 represses HIV-1 transcription and is regulated by HIV-1 Vpr and cellular DNA damage responses.PLoS pathogens · 2021Article
- Nucleic Acid Immunity and DNA Damage Response: New Friends and Old Foes.Frontiers in immunology · 2021Review
- The Interplay of HIV-1 and Macrophages in Viral Persistence.Frontiers in microbiology · 2021Review
- Vpu modulates DNA repair to suppress innate sensing and hyper-integration of HIV-1.Nature microbiology · 2020Article
- The DNA Damage Response and HIV-Associated Pulmonary Arterial Hypertension.International journal of molecular sciences · 2020Review
- Review
- HIV-1 Vpr mediates the depletion of the cellular repressor CTIP2 to counteract viral gene silencing.Scientific reports · 2019Article
- Illuminating the Role of Vpr in HIV Infection of Myeloid Cells.Frontiers in immunology · 2019Review
- Identification of Inhibitors of the dNTP Triphosphohydrolase SAMHD1 Using a Novel and Direct High-Throughput Assay.Biochemistry · 2018Article
- HIV-1 Vpr hijacks EDD-DYRK2-DDB1The Journal of biological chemistry · 2018Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viruses have been long known to perturb cell cycle regulators and key players of the DNA damage response to benefit their life cycles. In the case of the human immunodeficiency virus (HIV), the viral auxiliary protein Vpr activates the structure-specific endonuclease SLX4 complex to promote escape from innate immune sensing and, as a side effect, induces replication stress in cycling cells and subsequent cell cycle arrest at the G2/M transition. This novel pathway subverted by HIV to prevent accumulation of viral reverse transcription by-products adds up to facilitating effects of major cellular exonucleases that degrade pathological DNA species. Within this review we discuss the impact of this finding on our understanding of the interplay between HIV replication and nucleic acid metabolism and its implications for cancer-related chronic inflammation.
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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.