ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Human immunodeficiency virus infection of human astrocytes disrupts blood-brain barrier integrity by a gap junction-dependent mechanism.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 papers, 1 of them a synthesis that pooled it.
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Who cites it
182 citing papers in PubMed, 1 synthesis or guideline pooled it, 249 citations in OpenAlex.
- Implications and prospects of immunological and neuroimaging research in HIV-associated neurocognitive disorders.Frontiers in neurologyPooled it
- Molecular Signatures of HIV-Induced Neuroinflammation and Neurodegeneration in Human Cerebral Organoids: Identification of Therapeutic Targets for NeuroHIV.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Latent HIV Infection of BBB Pericytes Enhances Gap Junction-mediated Crosstalk with Endothelial Cells.Molecular neurobiology · 2026Article
- HAND in Africa: prevalence, diagnostic challenges and the search for objective markers.Journal of neurovirology · 2026Review
- Soluble TREM2 Mediates Blood Brain Barrier Permeability through Astrocyte Reactivity.Research square · 2026Article
- Latent HIV Infection of BBB Pericytes Disrupts Gap Junction-Mediated Crosstalk with Endothelial Cells.Research square · 2026Article
- Inhibiting glycan degradation prevents HIV-induced inflammaging and cognitive impairment.Med (New York, N.Y.) · 2026Article
- Astrocytoma in Patients with HIV-Review of the Literature and Case Report.Pathogens (Basel, Switzerland) · 2026Review
- Review
- Deceiving the gatekeepers: virus modulation of gap junctions.Microbiology and molecular biology reviews : MMBR · 2025Review
- Inhibiting Glycan Degradation Prevents HIV-Induced Inflammaging and Cognitive Impairment.bioRxiv : the preprint server for biology · 2025Article
- Cerebrospinal Fluid Biomarkers in Opioid Dependence: Evidence of Neuroimmune Activation and Ion Composition Changes, Without Alteration in Orexin-A.Addiction biology · 2025Article
- Review
- New perspectives on heterogeneity in astrocyte reactivity in neuroinflammation.Brain, behavior, & immunity - health · 2025Article
- HIV Cerebrospinal Fluid Escape: Interventions for the Management, Current Evidence and Future Perspectives.Tropical medicine and infectious disease · 2025Review
- SIV infection induces alterations in gene expression and loss of interneurons in Rhesus Macaque frontal cortex during early systemic infection.Translational psychiatry · 2025Article
- Drug Delivery Across the Blood-Brain Barrier: A New Strategy for the Treatment of Neurological Diseases.Pharmaceutics · 2024Review
- The challenges to detect, quantify, and characterize viral reservoirs in the current antiretroviral era.NeuroImmune pharmacology and therapeutics · 2024Review
- Uncovering chikungunya virus-encoded miRNAs and host-specific targeted genes associated with antiviral immune responses: an integrated bioinformatics approach.Scientific reports · 2024Article
- Human Brain In Vitro Model for Pathogen Infection-Related Neurodegeneration Study.International journal of molecular sciences · 2024Review
122 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
HIV infection of the CNS is an early event after primary infection, resulting in neurological complications in a significant number of individuals despite antiretroviral therapy (ART). The main cells infected with HIV within the CNS are macrophages/microglia and a small fraction of astrocytes. The role of these few infected astrocytes in the pathogenesis of neuroAIDS has not been examined extensively. Here, we demonstrate that few HIV-infected astrocytes (4.7 ± 2.8% in vitro and 8.2 ± 3.9% in vivo) compromise blood-brain barrier (BBB) integrity. This BBB disruption is due to endothelial apoptosis, misguided astrocyte end feet, and dysregulation of lipoxygenase/cyclooxygenase, BK(Ca) channels, and ATP receptor activation within astrocytes. All of these alterations in BBB integrity induced by a few HIV-infected astrocytes were gap junction dependent, as blocking these channels protected the BBB from HIV-infected astrocyte-mediated compromise. We also demonstrated apoptosis in vivo of BBB cells in contact with infected astrocytes using brain tissue sections from simian immunodeficiency virus-infected macaques as a model of neuroAIDS, suggesting an important role for these few infected astrocytes in the CNS damage seen with HIV infection. Our findings describe a novel mechanism of bystander BBB toxicity mediated by low numbers of HIV-infected astrocytes and amplified by gap junctions. This mechanism of toxicity contributes to understanding how CNS damage is spread even in the current ART era and how minimal or controlled HIV infection still results in cognitive impairment in a large population of infected individuals.
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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.