ArticleGlia2005
HIV-1 tat protein induces a migratory phenotype in human fetal microglia by a CCL2 (MCP-1)-dependent mechanism: possible role in NeuroAIDS.
Article in Glia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 77 citations in OpenAlex.
- Article
- Article
- Human Brain Endothelial Cell-Derived Extracellular Vesicles ReduceInternational journal of molecular sciences · 2025Article
- The Clinical Application of Pulsed Radiofrequency Induces Inflammatory Pain via MAPKs Activation: A Novel Hint for Pulsed Radiofrequency Treatment.International journal of molecular sciences · 2021Article
- Co-receptor signaling in the pathogenesis of neuroHIV.Retrovirology · 2021Review
- GPR18 drives FAAH inhibition-induced neuroprotection against HIV-1 Tat-induced neurodegeneration.Experimental neurology · 2021Article
- Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind.Cancers · 2021Review
- HIV-1 Tat: Role in Bystander Toxicity.Frontiers in cellular and infection microbiology · 2020Review
- The Role of Chemokines in the Pathophysiology of Major Depressive Disorder.International journal of molecular sciences · 2019Review
- The role of connexin and pannexin containing channels in the innate and acquired immune response.Biochimica et biophysica acta. Biomembranes · 2018Review
- HIV-infected macrophages and microglia that survive acute infection become viral reservoirs by a mechanism involving Bim.Scientific reports · 2017Article
- Differential host gene responses from infection with neurovirulent and partially-neurovirulent strains of Venezuelan equine encephalitis virus.BMC infectious diseases · 2017Article
- Review
- A multispecies approach for understanding neuroimmune mechanisms of stress.Dialogues in clinical neuroscience · 2017Review
- HIV-tat alters Connexin43 expression and trafficking in human astrocytes: role in NeuroAIDS.Journal of neuroinflammation · 2016Article
- A Potential Contribution of Chemokine Network Dysfunction to the Depressive Disorders.Current neuropharmacology · 2016Review
- Fractalkine Attenuates Microglial Cell Activation Induced by Prenatal Stress.Neural plasticity · 2016Article
- Effect of human immunodeficiency virus on blood-brain barrier integrity and function: an update.Frontiers in cellular neuroscience · 2015Review
- Cannabinoid inhibits HIV-1 Tat-stimulated adhesion of human monocyte-like cells to extracellular matrix proteins.Life sciences · 2014Article
- Interactions of HIV and drugs of abuse: the importance of glia, neural progenitors, and host genetic factors.International review of neurobiology · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Acquired immune deficiency syndrome (AIDS) encephalitis and dementia are characterized by neuronal loss, astrogliosis, and microglia activation and migration that contribute to the formation of multinucleated giant cells. Despite extensive evidence of pathological changes in the brain of infected individuals, the mechanisms of human immune deficiency virus type 1 (HIV-1) entry, microglia migration, and viral propagation within the brain are still not completely understood. In this study, we report that the induction of a migratory phenotype in human fetal microglia by the HIV-1 transactivator protein, tat, is mediated by the chemokine, CCL2. CCL2 or tat treatment alone induced rearrangement of actin and the formation of microglial processes. The time course of cell membrane ruffling induced by CCL2 was faster (5-30 min) than that elicited by tat treatment (2-3 h). Our previous data in human fetal microglia showed that tat induces CCL2 expression. Thus, we examined whether tat-induced microglia membrane ruffling and process formation, critical components in cell migration, are mediated by the secretion of CCL2 by these cells. To test this hypothesis, we treated microglia with tat protein in the presence of neutralizing CCL2 antibodies. Co-treatment with neutralizing CCL2 antibodies resulted in the loss of tat-induced membrane ruffling. Tat treatment of microglia induced polarization of CCR2, the receptor for CCL2, to the leading edge of processes, further suggesting a CCL2-dependent mechanism of tat-induced microglia migration. Our data indicate that tat facilitates microglia migration by inducing autocrine CCL2 release. Our results suggest that tat induced CCL2 secretion may be one of the early signals during NeuroAIDS.
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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.