ReviewJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2012
Delineating HIV-associated neurocognitive disorders using transgenic models: the neuropathogenic actions of Vpr.
Review in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- The Complex Interactions Between HIV-1 and Human Host Cell Genome: From Molecular Mechanisms to Clinical Practice.International journal of molecular sciences · 2025Review
- Correlation of HIV-Induced Neuroinflammation and Synaptopathy with Impairment of Learning and Memory in Mice with HAND.Journal of clinical medicine · 2023Article
- Alzheimer's-Like Pathology at the Crossroads of HIV-Associated Neurological Disorders.Vaccines · 2021Review
- Article
- Potential pharmacological approaches for the treatment of HIV-1 associated neurocognitive disorders.Fluids and barriers of the CNS · 2020Review
- Simultaneous determination of intracellular concentrations of tenofovir, emtricitabine, and dolutegravir in human brain microvascular endothelial cells using liquid chromatography-tandem mass spectrometry (LC-MS/MS).Analytica chimica acta · 2019Article
- Structural alteration of DNA induced by viral protein R of HIV-1 triggers the DNA damage response.Retrovirology · 2018Article
- HIV-1 matrix protein p17 misfolding forms toxic amyloidogenic assemblies that induce neurocognitive disorders.Scientific reports · 2017Article
- HIV-1 Viral Protein R Activates NLRP3 Inflammasome in Microglia: implications for HIV-1 Associated Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Article
- HIV-associated neurocognitive disorders: recent advances in pathogenesis, biomarkers, and treatment.F1000Research · 2017Review
- Neuroinflammation-Induced Interactions between Protease-Activated Receptor 1 and Proprotein Convertases in HIV-Associated Neurocognitive Disorder.Molecular and cellular biology · 2015Article
- Oligodendrocytes Are Targets of HIV-1 Tat: NMDA and AMPA Receptor-Mediated Effects on Survival and Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Vpr expression abolishes the capacity of HIV-1 infected cells to repair uracilated DNA.Nucleic acids research · 2014Article
- Enhanced human immunodeficiency virus Type 1 expression and neuropathogenesis in knockout mice lacking Type I interferon responses.Journal of neuropathology and experimental neurology · 2014Article
- Targeting the glutamatergic system for the treatment of HIV-associated neurocognitive disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013Review
- Article
- Article
- Neuronal apoptosis by HIV-1 Vpr: contribution of proinflammatory molecular networks from infected target cells.Journal of neuroinflammation · 2012Article
- Commentary: Animal models of neuroAIDS.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012Article
- Rodent models for HIV-associated neurocognitive disorders.Trends in neurosciences · 2012Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV-associated neurocognitive disorders (HAND) represent a constellation of neurological disabilities defined by neuropsychological impairments, neurobehavioral abnormalities and motor deficits. To gain insights into the mechanisms underlying the development of these disabilities, several transgenic models have been developed over the past two decades, which have provided important information regarding the cellular and molecular factors contributing to the neuropathogenesis of HAND. Herein, we concentrate on the neuropathogenic effects of HIV-1 Vpr expressed under the control of c-fms, resulting transgene expression in myeloid cells in both the central and peripheral nervous systems. Vpr's actions, possibly through its impact on cell cycle machinery, in brain culminate in neuronal and astrocyte injury and death through apoptosis involving activation of caspases-3, -6 and -9 depending on the individual target cell type. Indeed, these outcomes are also induced by soluble Vpr implying Vpr's effects stem from direct interaction with target cells. Remarkably, in vivo transgenic Vpr expression induces a neurodegenerative phenotype defined by neurobehavioral deficits and neuronal loss in the absence of frank inflammation. Implantation of another viral protein, hepatitis C virus (HCV) core, into Vpr transgenic animals' brains stimulated neuroinflammation and amplified the neurodegenerative disease phenotype, thereby recapitulating HCV's putative neuropathogenic actions. The availability of different transgenic models to study HIV neuropathogenesis represents exciting and innovative approaches to understanding disease mechanisms and perhaps developing new therapeutic strategies in the future.
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