ArticlePloS one2021
Direct interaction of HIV gp120 with neuronal CXCR4 and CCR5 receptors induces cofilin-actin rod pathology via a cellular prion protein- and NOX-dependent mechanism.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- HIV-1 gp120-induced lysosomal stress responses are controlled by TRPML1 redox sensors.Redox report : communications in free radical research · 2026Article
- Viral Comorbidities Remodel Host Transcriptome and Redox Signaling in an NADPH Oxidase Isoform-Specific Manner.Viruses · 2026Review
- Review
- HIV-1 gp120-induced lysosomal stress responses are controlled by TRPML1 redox sensors.bioRxiv : the preprint server for biology · 2026Article
- HIV-Induced Apoptosis: Host Defense and Viral Strategy.Biology · 2025Review
- Human endogenous retrovirus W family envelope protein (ERVWE1) regulates macroautophagy activation and micromitophagy inhibition via NOXA1 in schizophrenia.Virologica Sinica · 2025Article
- Neuropathogenesis of acute HIV: mechanisms, biomarkers, and therapeutic approaches.Current opinion in HIV and AIDS · 2025Review
- Cofilin(s) and Mitochondria: Function Beyond Actin Dynamics.International journal of molecular sciences · 2025Review
- The contributing role of CCR5 in dementia.Frontiers in neurology · 2025Review
- ROS Chronicles in HIV Infection: Genesis of Oxidative Stress, Associated Pathologies, and Therapeutic Strategies.Current issues in molecular biology · 2024Review
- α-Synuclein triggers cofilin pathology and dendritic spine impairment via a PrPCell death & disease · 2024Article
- The chemokine receptor CCR5: multi-faceted hook for HIV-1.Retrovirology · 2024Review
- Chemokine Receptor Antagonists Prevent and Reverse Cofilin-Actin Rod Pathology and Protect Synapses in Cultured Rodent and Human iPSC-Derived Neurons.Biomedicines · 2024Article
- Characterization of a Human Neuronal Culture System for the Study of Cofilin-Actin Rod Pathology.Biomedicines · 2023Article
- The Impact of Neurotransmitters on the Neurobiology of Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Potential molecular mechanisms of chronic fatigue in long haul COVID and other viral diseases.Infectious agents and cancer · 2023Review
- HIV-1 envelope protein gp120 modulation of glutamate effects on cortical neuronal synapses: implications for HIV-1-associated neuropathogenesis.International journal of physiology, pathophysiology and pharmacology · 2023Article
- Identification of human immunodeficiency virus -1 E protein-targeting lead compounds by pharmacophore based screening.Saudi medical journal · 2022Article
- Review
- Metabolic Reprogramming in HIV-Associated Neurocognitive Disorders.Frontiers in cellular neuroscience · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Nearly 50% of individuals with long-term HIV infection are affected by the onset of progressive HIV-associated neurocognitive disorders (HAND). HIV infiltrates the central nervous system (CNS) early during primary infection where it establishes persistent infection in microglia (resident macrophages) and astrocytes that in turn release inflammatory cytokines, small neurotoxic mediators, and viral proteins. While the molecular mechanisms underlying pathology in HAND remain poorly understood, synaptodendritic damage has emerged as a hallmark of HIV infection of the CNS. Here, we report that the HIV viral envelope glycoprotein gp120 induces the formation of aberrant, rod-shaped cofilin-actin inclusions (rods) in cultured mouse hippocampal neurons via a signaling pathway common to other neurodegenerative stimuli including oligomeric, soluble amyloid-β and proinflammatory cytokines. Previous studies showed that synaptic function is impaired preferentially in the distal proximity of rods within dendrites. Our studies demonstrate gp120 binding to either chemokine co-receptor CCR5 or CXCR4 is capable of inducing rod formation, and signaling through this pathway requires active NADPH oxidase presumably through the formation of superoxide (O2-) and the expression of cellular prion protein (PrPC). These findings link gp120-mediated oxidative stress to the generation of rods, which may underlie early synaptic dysfunction observed in HAND.
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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.