ArticleRetrovirology2014
Rapid inflammasome activation in microglia contributes to brain disease in HIV/AIDS.
Article in Retrovirology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 1 of them a synthesis that pooled it.
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Who cites it
154 citing papers in PubMed, 1 synthesis or guideline pooled it, 239 citations in OpenAlex.
- Mechanisms and treatments of methamphetamine and HIV-1 co-induced neurotoxicity: a systematic review.Frontiers in immunology · 2024Pooled it
- Flagellin/NLRC4 Pathway Rescues NLRP3-Inflammasome Defect in Dendritic Cells From HIV-Infected Patients: Perspective for New Adjuvant in Immunocompromised Individuals.Frontiers in immunology · 2019Trial
- Distinct Transcriptomic Signatures of HIV-1 Tat and gp120 Uncover Differential Neuroimmune Vulnerability in aCurrent issues in molecular biology · 2026Article
- Smoldering in the sanctuary: HIV-associated brain injury in the ART era.The Journal of clinical investigation · 2026Review
- Transcriptomic Profiling Identifies TALAM1 and LINC00702 as HIV-1-Responsive lncRNAs in Microglia.International journal of molecular sciences · 2026Article
- Neuroinflammation and NeuroHIV: understanding the role of HIV-1 related factors in microglial activation.Translational psychiatry · 2026Review
- Brain and neural cell type proteomics reveal extracellular matrix proteins enriched in progressive multiple sclerosis.Nature communications · 2026Article
- Delivery of Nerve Growth Factor via Exosome Attenuates Neuropathic Pain in a Rat Model of Chronic Constriction Injury.Current neuropharmacology · 2026Article
- Persistent activation of monocytes/macrophages and cell senescence in SIV-infected macaques on ART.Frontiers in immunology · 2026Article
- The prefrontal cortex as a target of HIV-1 neurotoxicity: molecular mechanisms of viral protein-mediated neurodegeneration and executive dysfunction.Frontiers in cellular neuroscience · 2026Review
- Investigation of CNS damage following HIV infection and methamphetamine exposure using human iPSC-derived microglia and 3D cerebral assembloid models.bioRxiv : the preprint server for biology · 2025Article
- HIV-1 Tat Protein Exposure Alters the Morphological Characteristics and Gene Expression in the Primary Mouse Cortex Endothelial Cells and Human Brain Microvascular Endothelial Cells.Cellular and molecular neurobiology · 2025Article
- Th2 cell-derived exosomes alleviate central nervous system inflammation and demyelination in experimental autoimmune encephalomyelitis by regulating inflammasomes to inhibit microglia activation.Molecular biology reports · 2025Article
- Persistent Activation of Monocytes/Macrophages and Cell Senescence in SIV-Infected Macaques on ART.bioRxiv : the preprint server for biology · 2025Article
- HIV-1 Tat protein exposure alters the morphological characteristics and gene expression in the primary mouse cortex endothelial cells and human brain microvascular endothelial cells.Research square · 2025Article
- Differential Effects of Cannabinoid Receptor 2 Agonists on HIV Replication and Inflammatory Activation in Monocyte-Derived Macrophages and Induced Pluripotent Stem Cell-Derived Microglia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Methamphetamine and HIV-1 Tat Synergistically Induce Microglial Pyroptosis Via Activation of the AIM2 Inflammasome.Inflammation · 2025Article
- Expression of intron-containing HIV-1 RNA induces NLRP1 inflammasome activation in myeloid cells.PLoS biology · 2025Article
- Article
- Innate immune mechanisms of infection: what we know and potential conserved mechanisms affecting sleep during infection.Neurobiology of sleep and circadian rhythms · 2025Article
94 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHuman immunodeficiency virus type 1(HIV-1) infects and activates innate immune cells in the brain resulting in inflammation and neuronal death with accompanying neurological deficits. Induction of inflammasomes causes cleavage and release of IL-1β and IL-18, representing pathogenic processes that underlie inflammatory diseases although their contribution HIV-associated brain disease is unknown.
resultsInvestigation of inflammasome-associated genes revealed that IL-1β, IL-18 and caspase-1 were induced in brains of HIV-infected persons and detected in brain microglial cells. HIV-1 infection induced pro-IL-1β in human microglia at 4 hr post-infection with peak IL-1β release at 24 hr, which was accompanied by intracellular ASC translocation and caspase-1 activation. HIV-dependent release of IL-1β from a human macrophage cell line, THP-1, was inhibited by NLRP3 deficiency and high extracellular [K+]. Exposure of microglia to HIV-1 gp120 caused IL-1β production and similarly, HIV-1 envelope pseudotyped viral particles induced IL-1β release, unlike VSV-G pseudotyped particles. Infection of cultured feline macrophages by the related lentivirus, feline immunodeficiency virus (FIV), also resulted in the prompt induction of IL-1β. In vivo FIV infection activated multiple inflammasome-associated genes in microglia, which was accompanied by neuronal loss in cerebral cortex and neurological deficits. Multivariate analyses of data from FIV-infected and uninfected animals disclosed that IL-1β, NLRP3 and caspase-1 expression in cerebral cortex represented key molecular determinants of neurological deficits.
conclusionsNLRP3 inflammasome activation was an early and integral aspect of lentivirus infection of microglia, which was associated with lentivirus-induced brain disease. Inflammasome activation in the brain might represent a potential target for therapeutic interventions in HIV/AIDS.
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