ArticleNature communications2018
HIV-1 intron-containing RNA expression induces innate immune activation and T cell dysfunction.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 90 citations in OpenAlex.
- Multivariate Computational Analysis of Gamma Delta T Cell Inhibitory Receptor Signatures Reveals the Divergence of Healthy and ART-Suppressed HIV+ Aging.Frontiers in immunology · 2018Trial
- Intragenic transcription from defective HIV proviruses triggers interferon responses in myeloid cells.Journal of virology · 2026Article
- Transcription start site heterogeneity controls MDA5 sensing of unspliced HIV-1 RNAs.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A tissue-intrinsic mechanism sensitizes HIV-1 particles for TLR-triggered innate immune responses.Nature communications · 2026Article
- Intragenic Transcription from Defective HIV Proviruses Triggers Interferon Responses in Myeloid Cells.bioRxiv : the preprint server for biology · 2026Article
- Neuroinflammation and NeuroHIV: understanding the role of HIV-1 related factors in microglial activation.Translational psychiatry · 2026Review
- Tools to Quantify and Characterize the Persistent Reservoir in People with HIV-1: Focus on Non-B Subtypes.Viruses · 2026Review
- Modulation of IRF7-driven transcription as a strategy to control HIV-1 latency.Frontiers in immunology · 2026Article
- NF-κB-dependent and independent inflammatory responses during acute HIV-1 infection in a model of human microglia.Frontiers in immunology · 2026Article
- The effect of combining HIV latency reversal with inhibition of phosphoinositide-3 kinases or B-cell lymphoma-2 on the HIV reservoir.PLoS pathogens · 2026Article
- Nef stabilizes actin to prevent HIV-1 sensing by RIG-I-like receptors.Nature communications · 2025Article
- Evasion of CARD8 activation during HIV-1 assembly.Science advances · 2025Article
- Incorporation of 5-methylcytidine alleviates RIG-I-mediated innate immune responses to a self-amplifying RNA vaccine.Science translational medicine · 2025Article
- A scalable proteogenomic framework for dissecting phospho-signaling pathways in primary immune cells.bioRxiv : the preprint server for biology · 2025Article
- Expression of intron-containing HIV-1 RNA induces NLRP1 inflammasome activation in myeloid cells.PLoS biology · 2025Article
- 5' cap sequestration is required for sensing of unspliced HIV-1 RNA by MDA5.bioRxiv : the preprint server for biology · 2025Article
- MrHAMER2: high-accuracy long-read RNA sequencing to decode isoform-specific variation in viral transcripts during latency.bioRxiv : the preprint server for biology · 2025Article
- Cell-free assays reveal that the HIV-1 capsid protects reverse transcripts from cGAS immune sensing.PLoS pathogens · 2025Article
- Mu opioid receptor activation in microglia enhances HIV-1 infection and HIV-infection-induced inflammatory responses.Frontiers in immunology · 2025Article
- Intracellular HIV-1 Tat regulator induces epigenetic changes in the DNA methylation landscape.Frontiers in immunology · 2025Article
7 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
6 authors at 1 institution in 1 country.
Funding
Abstract
Low levels of type I interferon (IFN-I) are thought to be a driving force for immune activation and T-cell exhaustion in HIV-1 infected individuals on combination antiretroviral therapy (cART), though the causative mechanisms for persistent IFN-I signaling have remained unclear. Here, we show Rev-CRM1-dependent nuclear export and peripheral membrane association of intron-containing HIV-1 RNA, independent of primary viral sequence or viral protein expression, is subject to sensing and signaling via MAVS, resulting in IFN-I-dependent pro-inflammatory responses in macrophages. Additionally, HIV-1 intron-containing-RNA-induced innate immune activation of macrophages leads to upregulation of inhibitory receptor expression and functional immune exhaustion of co-cultured T cells. Our findings suggest that persistent expression of HIV-1 intron-containing RNA in macrophages contributes to chronic immune activation and T-cell dysfunction and that use of HIV RNA expression inhibitors as adjunct therapy might abrogate aberrant inflammation and restore immune function in HIV-infected individuals on cART.
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.