ReviewJournal of virology2015
MAVS Coordination of Antiviral Innate Immunity.
Review in Journal of virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 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
120 citing papers in PubMed, 181 citations in OpenAlex.
- Establishing the molecular basis for MDA5 mutation-linked autoimmunity.Nucleic acids research · 2026Article
- The factory enters the fray: how mitochondrial protein trafficking shapes the host response to infection.Journal of virology · 2026Review
- Cyclo-C stabilizes PEX13 to inhibit porcine epidemic diarrhea virus replication by blocking pexophagy-mediated disruption of antiviral innate immunity.Journal of virology · 2026Article
- Weakened macrophage antibacterial capacity in myelodysplastic syndrome.ImmunoHorizons · 2026Article
- Biallelic variants inResearch square · 2026Article
- MAVS as a Key Regulator of Tumor Proliferation, Survival, the Tumor Microenvironment, and Immunity.Biomolecules · 2026Article
- Prion-like MAVS fibrils stitch mitochondria to promote a rapid antiviral response.Cellular & molecular immunology · 2026Article
- Bovine viral diarrhea virus suppresses type I IFN production by inducing MAVS degradation via autophagy mediated by the ROS-endoplasmic reticulum stress axis.Journal of virology · 2026Article
- The molecular mechanisms of autophagy-virus interactions: from antiviral defense to viral counterstrategies.FEMS microbiology reviews · 2026Review
- Post-translational control of MAVS signaling: linking mitochondrial antiviral immunity to metabolic and cellular stress contexts.Frontiers in physiology · 2026Review
- Targeting Host Dependency Factors: A Paradigm Shift in Antiviral Strategy Against RNA Viruses.International journal of molecular sciences · 2025Review
- Biological and clinical implications of a model of surveillance immunity.The Journal of clinical investigation · 2025Review
- Metabolic Reprogramming in Respiratory Viral Infections: A Focus on SARS-CoV-2, Influenza, and Respiratory Syncytial Virus.Biomolecules · 2025Review
- Shaping the composition of the mitochondrial outer membrane.Nature cell biology · 2025Review
- Innate Immune Sensors and Cell Death-Frontiers Coordinating Homeostasis, Immunity, and Inflammation in Skin.Viruses · 2025Review
- Identification of mitochondrial related gene characteristics and potential molecular mechanism of acute otitis media.Frontiers in molecular biosciences · 2025Article
- Cellular RNA interacts with MAVS to promote antiviral signaling.Science (New York, N.Y.) · 2024Article
- Characterization of Freshly Isolated Human Peripheral Blood B Cells, Monocytes, CD4+ and CD8+ T Cells, and Skin Mast Cells by Quantitative Transcriptomics.International journal of molecular sciences · 2024Article
- Usutu virus NS4A suppresses the host interferon response by disrupting MAVS signaling.Virus research · 2024Article
- Post-Acute Sequelae and Mitochondrial Aberration in SARS-CoV-2 Infection.International journal of molecular sciences · 2024Review
60 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
2 authors at 1 institution in 1 country.
Funding
Abstract
RNA virus infection is sensed in the cytoplasm by the retinoic acid-inducible gene I (RIG-I)-like receptors. These proteins signal through the host adaptor protein MAVS to trigger the antiviral innate immune response. Here, we describe how MAVS subcellular localization impacts its function and the regulation underlying MAVS signaling. We propose a model to describe how the coordination of MAVS functions at the interface between the mitochondria and the mitochondrion-associated endoplasmic reticulum (ER) membrane programs antiviral signaling.
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.