ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Gap junctions mediate human immunodeficiency virus-bystander killing in astrocytes.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
What it found
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Who cites it
103 citing papers in PubMed, 127 citations in OpenAlex.
- Beyond the neuron: the role of glial cells in viral neuropathogenesis.Journal of virology · 2026Review
- Deceiving the gatekeepers: virus modulation of gap junctions.Microbiology and molecular biology reviews : MMBR · 2025Review
- Viral Infection and Connexin Dysfunction in the Heart.Current cardiology reports · 2025Review
- SIV infection induces alterations in gene expression and loss of interneurons in Rhesus Macaque frontal cortex during early systemic infection.Translational psychiatry · 2025Article
- Coordination of innate immune responses by connexins.Frontiers in immunology · 2025Review
- The challenges to detect, quantify, and characterize viral reservoirs in the current antiretroviral era.NeuroImmune pharmacology and therapeutics · 2024Review
- Cenicriviroc prevents dysregulation of astrocyte/endothelial cross talk induced by ischemia and HIV-1 via inhibiting the NLRP3 inflammasome and pyroptosis.American journal of physiology. Cell physiology · 2024Article
- Mechanisms of Intracellular Communication in Cancer and Pathogen Spreading.Results and problems in cell differentiation · 2024Review
- Chronic brain damage in HIV-infected individuals under antiretroviral therapy is associated with viral reservoirs, sulfatide release, and compromised cell-to-cell communication.Cellular and molecular life sciences : CMLS · 2023Article
- Mechanisms of Zika astrocyte infection and neuronal toxicity.NeuroImmune pharmacology and therapeutics · 2023Article
- Shock and kill within the CNS: A promising HIV eradication approach?Journal of leukocyte biology · 2022Review
- Identification, Quantification, and Characterization of HIV-1 Reservoirs in the Human Brain.Cells · 2022Article
- Single-Cell RNA-Sequencing: Astrocyte and Microglial Heterogeneity in Health and Disease.Cells · 2022Review
- Neuropathy in Human Immunodeficiency Virus: A Review of the Underlying Pathogenesis and Treatment.Cureus · 2022Review
- Direct Cell-Cell Communication via Membrane Pores, Gap Junction Channels, and Tunneling Nanotubes: Medical Relevance of Mitochondrial Exchange.International journal of molecular sciences · 2022Review
- The role of Pannexin-1 channels and extracellular ATP in the pathogenesis of the human immunodeficiency virus.Purinergic signalling · 2021Review
- HIV infection of astrocytes compromises inter-organelle interactions and inositol phosphate metabolism: A potential mechanism of bystander damage and viral reservoir survival.Progress in neurobiology · 2021Article
- HIV-1 Tat and cocaine impact astrocytic energy reservoir influence on miRNA epigenetic regulation.Genomics · 2021Article
- Co-receptor signaling in the pathogenesis of neuroHIV.Retrovirology · 2021Review
- Astrocytes are HIV reservoirs in the brain: A cell type with poor HIV infectivity and replication but efficient cell-to-cell viral transfer.Journal of neurochemistry · 2021Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Human immunodeficiency virus (HIV) entry into the CNS is an early event after infection, resulting in neurological dysfunction in a significant number of individuals. As people with acquired immunodeficiency syndrome (AIDS) live longer, the prevalence of cognitive impairment is increasing, despite antiretroviral therapy. The mechanisms that mediate CNS dysfunction are still not completely understood, and include inflammation, viral presence, and/or replication. In this report, we characterize a novel role of gap junctions in transmitting and thereby amplifying toxic signals originating from HIV-infected astrocytes that trigger cell death in uninfected astrocytes. HIV-infected astrocytes were resistant to apoptosis; however, uninfected astrocytes forming gap junctions with infected astrocytes were apoptotic. Gap junction blockers abolished apoptosis in uninfected astrocytes, supporting the role of these channels in amplifying cell death. Our findings describe a novel mechanism of toxicity within the brain, triggered by low numbers of HIV-infected astrocytes and amplified by gap junctions, contributing to the pathogenesis of NeuroAIDS.
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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.