ArticleNature immunology2017
HIV-1 blocks the signaling adaptor MAVS to evade antiviral host defense after sensing of abortive HIV-1 RNA by the host helicase DDX3.
Article in Nature immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 82 papers.
What it found
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Who cites it
82 citing papers in PubMed, 136 citations in OpenAlex.
- HIV DNA and transcription before and after ART in natural controllers compared to noncontrollers.Journal of virology · 2026Article
- E3 ubiquitin ligase trim36 targets ddx3x for degradation to reprogram macrophage polarization and ameliorate tubal factor infertility in rats.Cell biology and toxicology · 2026Article
- Transcriptomic Signatures of Immune Suppression and Cellular Dysfunction Distinguish Latent from Transcriptionally Active HIV-1 Infection in Dendritic Cells.International journal of molecular sciences · 2026Article
- The USP1-WDR48 deubiquitinase complex functions as a molecular switch regulating tumor-associated macrophage activation and anti-tumor response.Cell death and differentiation · 2026Article
- At the crossroads of immunity and hijacking: dual roles of DDX proteins during host-virus interactions.Frontiers in cellular and infection microbiology · 2026Review
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
- Comparative Transcriptomics Analyses Identify DDX43 as a Cellular Regulator Involved in Suppressing HSV-2 Replication.Viruses · 2025Article
- HIV-1 latent infection modulates RNA sensors and innate immunity signaling in human brain pericytes.Research square · 2025Article
- Differential decreases in various HIV DNA regions and HIV transcripts after ART initiation during chronic infection.Journal of virology · 2025Article
- Genetic Variants in the NOD-like Receptor Signaling Pathway Are Associated with HIV-1/AIDS in a Northern Chinese Population.International journal of molecular sciences · 2025Article
- Equine lentivirus Gag protein degrades mitochondrial antiviral signaling protein via the E3 ubiquitin ligase Smurf1.Journal of virology · 2025Article
- DDX3X and virus interactions: functional diversity and antiviral strategies.Frontiers in microbiology · 2025Review
- Review
- Sterile activation of RNA-sensing pathways in autoimmunity.Journal of molecular cell biology · 2024Review
- DDX RNA helicases: key players in cellular homeostasis and innate antiviral immunity.Journal of virology · 2024Review
- PRRSV hijacks DDX3X protein and induces ferroptosis to facilitate viral replication.Veterinary research · 2024Article
- HIV-1 with gag processing defects activates cGAS sensing.Retrovirology · 2024Article
- Article
- IFNα Subtypes in HIV Infection and Immunity.Viruses · 2024Review
- Energy demanding RNA and protein metabolism drive dysfunctionality of HIV-specific T cell changes during chronic HIV infection.PloS one · 2024Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms by which human immunodeficiency virus 1 (HIV-1) avoids immune surveillance by dendritic cells (DCs), and thereby prevents protective adaptive immune responses, remain poorly understood. Here we showed that HIV-1 actively arrested antiviral immune responses by DCs, which contributed to efficient HIV-1 replication in infected individuals. We identified the RNA helicase DDX3 as an HIV-1 sensor that bound abortive HIV-1 RNA after HIV-1 infection and induced DC maturation and type I interferon responses via the signaling adaptor MAVS. Notably, HIV-1 recognition by the C-type lectin receptor DC-SIGN activated the mitotic kinase PLK1, which suppressed signaling downstream of MAVS, thereby interfering with intrinsic host defense during HIV-1 infection. Finally, we showed that PLK1-mediated suppression of DDX3-MAVS signaling was a viral strategy that accelerated HIV-1 replication in infected individuals.
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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.