ArticleThe Journal of biological chemistry2018
Methamphetamine increases HIV infectivity in neural progenitor cells.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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Who cites it
38 citing papers in PubMed, 47 citations in OpenAlex.
- Exercise-induced hippocampal miR-212/132 expression is preserved despite psychostimulant exposure and viral infection.Brain, behavior, and immunity · 2026Article
- Inhibiting glycan degradation prevents HIV-induced inflammaging and cognitive impairment.Med (New York, N.Y.) · 2026Article
- Methamphetamine enhances HIV infection of human iPSC-derived microglia.NeuroImmune pharmacology and therapeutics · 2026Article
- Recent Nanotherapeutic Advancements Against HIV-Associated Neurocognitive Disorders (HAND).Biomolecules · 2026Review
- Sigma-1 receptor regulates HIV-1 and methamphetamine-induced endothelial/pericyte barrier impairment via strain-specific inflammatory responses and mitochondrial dysregulation.Journal of neuroinflammation · 2026Article
- Inhibiting Glycan Degradation Prevents HIV-Induced Inflammaging and Cognitive Impairment.bioRxiv : the preprint server for biology · 2025Article
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- The Impact of HIV on Early Brain Aging-A Pathophysiological (Re)View.Journal of clinical medicine · 2024Review
- EcoHIV Infection of Primary Murine Brain Cell Cultures to Model HIV Replication and Neuropathogenesis.Viruses · 2024Article
- 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
- Human iPSC-derived brain organoids: A 3D mini-brain model for studying HIV infection.Experimental neurology · 2023Article
- CCL2 is required for initiation but not persistence of HIV infection mediated neurocognitive disease in mice.Scientific reports · 2023Article
- Chronic methamphetamine exposure exerts few effects on the iTat mouse model of HIV, but blocks Tat expression-induced slowed reward retrieval.Behavioural brain research · 2023Article
- Vision health perspectives onFrontiers in toxicology · 2023Review
- Astrocytes: Role in pathogenesis and effect of commonly misused drugs in the HIV infected brain.Current research in neurobiology · 2023Review
- Neutral sphingomyelinase 2 inhibition attenuates extracellular vesicle release and improves neurobehavioral deficits in murine HIV.Neurobiology of disease · 2022Article
- Characterization of basal ganglia volume changes in the context of HIV and polysubstance use.Scientific reports · 2022Article
- A Non-Canonical Role for IRE1α Links ER and Mitochondria as Key Regulators of Astrocyte Dysfunction: Implications in Methamphetamine use and HIV-Associated Neurocognitive Disorders.Frontiers in neuroscience · 2022Article
- Drugs of Abuse and Their Impact on Viral Pathogenesis.Viruses · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
HIV-1 infection and methamphetamine (METH) abuse frequently occur simultaneously and may have synergistic pathological effects. Although HIV-positive/active METH users have been shown to have higher HIV viral loads and experience more severe neurological complications than non-users, the direct impact of METH on HIV infection and its link to the development of neurocognitive alternations are still poorly understood. In the present study, we hypothesized that METH impacts HIV infection of neural progenitor cells (NPCs) by a mechanism encompassing NFκB/SP1-mediated HIV LTR activation. Mouse and human NPCs were infected with EcoHIV (modified HIV virus infectious to mice) and HIV, respectively, in the presence or absence of METH (50 or 100 μm). Pretreatment with METH, but not simultaneous exposure, significantly increased HIV production in both mouse and human NPCs. To determine the mechanisms underlying these effects, cells were transfected with different variants of HIV LTR promoters and then exposed to METH. METH treatment induced transcriptional activity of the HIV LTR promotor, an effect that required both NFκB and SP1 signaling. Pretreatment with METH also decreased neuronal differentiation of HIV-infected NPCs in both
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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.