ArticlePloS one2020
Herpes simplex virus type 1 inflammasome activation in proinflammatory human macrophages is dependent on NLRP3, ASC, and caspase-1.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Association between herpesviruses and alzheimer's disease: a meta-analysis based on case-control studies.Molecular and cellular biochemistry · 2025Pooled it
- Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026Review
- Macrophage makeover extreme viral edition: mechanisms of immune subversion and therapeutic perspectives.The Journal of general virology · 2026Review
- HSV-1 infections of the prefrontal cortex: regional vulnerability, cellular mechanisms, and neurocognitive consequences.Frontiers in cellular neuroscience · 2026Review
- Seborrhoea Herpeticum: A distinct entity or mere coincidence.Indian dermatology online journal · 2025Article
- Tackling cutaneous herpes simplex virus disease with topical immunomodulators-a call to action.Clinical microbiology reviews · 2025Review
- The Emerging Role of Colchicine to Inhibit NOD-like Receptor Family, Pyrin Domain Containing 3 Inflammasome and Interleukin-1β Expression in In Vitro Models.Biomolecules · 2025Article
- Tug of war: innate immunity and herpes simplex keratitis.Frontiers in immunology · 2025Review
- The dual roles of human PYHIN family proteins in cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Systemic immune challenge exacerbates neurodegeneration in a model of neurological lysosomal disease.EMBO molecular medicine · 2024Article
- Herpes Simplex Virus ICP27 Protein Inhibits AIM 2-Dependent Inflammasome Influencing Pro-Inflammatory Cytokines Release in Human Pigment Epithelial Cells (hTert-RPE 1).International journal of molecular sciences · 2024Article
- Overexpression of NLRP12 enhances macrophage immune response and alleviates herpes simplex keratitis.Frontiers in cellular and infection microbiology · 2024Article
- Advances in the mechanism of inflammasomes activation in herpes virus infection.Frontiers in immunology · 2024Review
- Korean Chestnut Honey Suppresses HSV-1 Infection by Regulating the ROS-NLRP3 Inflammasome Pathway.Antioxidants (Basel, Switzerland) · 2023Article
- IFI16 phase separation via multi-phosphorylation drives innate immune signaling.Nucleic acids research · 2023Article
- Chronic kidney disease and NLRP3 inflammasome: Pathogenesis, development and targeted therapeutic strategies.Biochemistry and biophysics reports · 2023Review
- Blue light irradiation exerts anti-viral and anti-inflammatory properties against herpes simplex virus type 1 infection.Journal of photochemistry and photobiology. B, Biology · 2023Article
- Article
- The innate and T-cell mediated immune response during acute and chronic gammaherpesvirus infection.Frontiers in cellular and infection microbiology · 2023Review
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The proinflammatory cytokines interleukin (IL)-1β and IL-18 are products of activation of the inflammasome, an innate sensing system, and important in the pathogenesis of herpes simplex virus type 1 (HSV-1). The release of IL-18 and IL-1β from monocytes/macrophages is critical for protection from HSV-1 based on animal models of encephalitis and genital infection, yet if and how HSV-1 activates inflammasomes in human macrophages is unknown. To investigate this, we utilized both primary human monocyte derived macrophages and human monocytic cell lines (THP-1 cells) with various inflammasome components knocked-out. We found that HSV-1 activates inflammasome signaling in proinflammatory primary human macrophages, but not in resting macrophages. Additionally, HSV-1 inflammasome activation in THP-1 cells is dependent on nucleotide-binding domain and leucine-rich repeat-containing receptor 3 (NLRP3), apoptosis-associated speck-like molecule containing a caspase recruitment domain (ASC), and caspase-1, but not on absent in melanoma 2 (AIM2), or gamma interferon-inducible protein 16 (IFI16). In contrast, HSV-1 activates non-canonical inflammasome signaling in proinflammatory macrophages that results in IL-1β, but not IL-18, release that is independent of NLRP3, ASC, and caspase-1. Ultraviolet irradiation of HSV-1 enhanced inflammasome activation, demonstrating that viral replication suppresses inflammasome activation. These results confirm that HSV-1 is capable of activating the inflammasome in human macrophages through an NLRP3 dependent process and that the virus has evolved an NLRP3 specific mechanism to inhibit inflammasome activation in macrophages.
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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.