ArticleThe American journal of pathology2010
Interactive comorbidity between opioid drug abuse and HIV-1 Tat: chronic exposure augments spine loss and sublethal dendritic pathology in striatal neurons.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
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Who cites it
118 citing papers in PubMed, 137 citations in OpenAlex.
- Neonatal intrahippocampal HIV-1 protein Tat(1-86) injection: neurobehavioral alterations in the absence of increased inflammatory cytokine activation.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2014Trial
- Cannabis use by people with HIV is associated with an anti-inflammatory immunometabolic phenotype in monocyte-derived macrophages.Journal of neuroinflammation · 2026Article
- IMPAIRED BRIDGING OF TEMPORAL DISCONTINUITIES IN OLDER ADULT HIV-1 TG RATS.bioRxiv : the preprint server for biology · 2026Article
- HIV-1 Tat expression drives progressive synaptic decline: evidence from longitudinal [NeuroImmune pharmacology and therapeutics · 2026Article
- Epigenetic mechanisms of HIV and opioid-induced neuropathology: Potential therapies and interventions.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- HIV-1 Tat protein alters medial prefrontal cortex neuronal activity and recognition memory.iScience · 2025Article
- Impact of HIV-1 tat protein on methamphetamine-induced inhibition of vesicular monoamine transporter2-mediated dopamine transport and methamphetamine conditioned place preference in HIV-1 tat transgenic mice.European journal of pharmacology · 2024Article
- The single-cell opioid responses in the context of HIV (SCORCH) consortium.Molecular psychiatry · 2024Article
- Examining the effects of the HIV-1 protein Tat and morphine on antiretroviral accumulation and distribution within the brain.Clinical and translational science · 2024Article
- Levetiracetam Prevents Neurophysiological Changes and Preserves Cognitive Function in the Human Immunodeficiency Virus (HIV)-1 Transactivator of Transcription Transgenic Mouse Model of HIV-Associated Neurocognitive Disorder.The Journal of pharmacology and experimental therapeutics · 2024Article
- HIV-Associated Neurocognitive Disorder: A Look into Cellular and Molecular Pathology.International journal of molecular sciences · 2024Review
- HIV-1 Tat and morphine interactions dynamically shift striatal monoamine levels and exploratory behaviors over time.Journal of neurochemistry · 2024Article
- Fentanyl dysregulates neuroinflammation and disrupts blood-brain barrier integrity in HIV-1 Tat transgenic mice.Journal of neurovirology · 2024Article
- A helping HAND: therapeutic potential of MAGL inhibition against HIV-1-associated neuroinflammation.Frontiers in immunology · 2024Article
- Advancing the preclinical study of comorbid neuroHIV and substance use disorders: Current perspectives and future directions.Brain, behavior, and immunity · 2023Review
- Therapeutically targeting the consequences of HIV-1-associated gastrointestinal dysbiosis: Implications for neurocognitive and affective alterations.Pharmacology, biochemistry, and behavior · 2023Article
- Differential Regulation of Tachykinin and Opioid System Gene Expression in Brain and Immune Cells of Chronic Binge Alcohol-Treated Simian Immunodeficiency Virus-Infected Macaques.AIDS research and human retroviruses · 2023Article
- Progressive Degeneration and Adaptive Excitability in Dopamine D1 and D2 Receptor-Expressing Striatal Neurons Exposed to HIV-1 Tat and Morphine.Cellular and molecular neurobiology · 2023Article
- Article
- Involvement of lncRNA TUG1 in HIV-1 Tat-Induced Astrocyte Senescence.International journal of molecular sciences · 2023Article
58 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
HIV-1 infection predisposes the central nervous system to damage by opportunistic infections and environmental insults. Such maladaptive plasticity may underlie the exaggerated comorbidity seen with HIV-1 infection and opioid abuse. Although morphine and HIV-1 Tat synergize at high concentrations to increase neuronal death in vitro, we questioned whether chronic low Tat exposure in vivo might contribute to the spectrum of neuropathology through sublethal neuronal injury. We used a doxycycline-driven, inducible, HIV-1 Tat transgenic mouse, in which striatal neuron death was previously shown to be absent, to examine effects of differential Tat expression, alone and combined with morphine. Low constitutive Tat expression caused neurodegeneration; higher levels induced by 7 days of doxycycline significantly reduced dendritic spine numbers. Moreover, Tat expression widely disrupted the endogenous opioid system, altering mu and kappa, but not delta, opioid receptor and proopiomelanocortin, proenkephalin, and prodynorphin transcript levels in cortex, hippocampus, and striatum. In addition to markedly reducing spine density by itself, morphine amplified the effect of higher levels of Tat on spines, and also potentiated Tat-mediated dendritic pathology, thus contributing to maladaptive neuroplasticity at multiple levels. The dendritic pathology and reductions in spine density suggest that sustained Tat +/- morphine exposure underlie key aspects of chronic neurodegenerative changes in neuroAIDS, which may contribute to the exacerbated neurological impairment in HIV patients who abuse opioids.
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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.