ArticleJournal of molecular biology2007
Infection of human immunodeficiency virus and intracellular viral Tat protein exert a pro-survival effect in a human microglial cell line.
Article in Journal of molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
36 citing papers in PubMed, 49 citations in OpenAlex.
- Review
- HMC3 revealed: how much do these "Microglia" really tell us?Frontiers in immunology · 2026Review
- HIV-Induced Apoptosis: Host Defense and Viral Strategy.Biology · 2025Review
- HIV-1-related factors interact with p53 to influence cellular processes.AIDS research and therapy · 2023Review
- Human microglial models to study HIV infection and neuropathogenesis: a literature overview and comparative analyses.Journal of neurovirology · 2022Review
- Human Immunodeficiency Virus Type 1 Vif Up-Regulates the Expression of TatFrontiers in microbiology · 2022Article
- Viral protein X reduces the incorporation of mutagenic noncanonical rNTPs during lentivirus reverse transcription in macrophages.The Journal of biological chemistry · 2020Article
- Inhibition of the lncRNA SAF drives activation of apoptotic effector caspases in HIV-1-infected human macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The human microglial HMC3 cell line: where do we stand? A systematic literature review.Journal of neuroinflammation · 2018Review
- Exosomal miR-9 Released from HIV Tat Stimulated Astrocytes Mediates Microglial Migration.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018Article
- In vitro and Ex vivo Neurotoxic Effects of Efavirenz are Greater than Those of Other Common Antiretrovirals.Neurochemical research · 2017Article
- HIV-1 Tat potently stabilises Mdm2 and enhances viral replication.The Biochemical journal · 2017Article
- Toll-like receptor 3 activation selectively reverses HIV latency in microglial cells.Retrovirology · 2017Article
- Immortalization of primary microglia: a new platform to study HIV regulation in the central nervous system.Journal of neurovirology · 2017Article
- Metabolic profiling during HIV-1 and HIV-2 infection of primary human monocyte-derived macrophages.Virology · 2016Article
- Combined antiretroviral therapy reduces brain viral load and pathological features of HIV encephalitis in a mouse model.Journal of neurovirology · 2014Article
- The phosphorylation of HIV-1 Gag by atypical protein kinase C facilitates viral infectivity by promoting Vpr incorporation into virions.Retrovirology · 2014Article
- High levels of CD2 expression identify HIV-1 latently infected resting memory CD4+ T cells in virally suppressed subjects.Journal of virology · 2013Article
- HIV-1 Tat C-mediated regulation of tumor necrosis factor receptor-associated factor-3 by microRNA 32 in human microglia.Journal of neuroinflammation · 2012Article
- WISP1 (CCN4) autoregulates its expression and nuclear trafficking of β-catenin during oxidant stress with limited effects upon neuronal autophagy.Current neurovascular research · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The interaction of human immunodeficiency virus type 1 (HIV-1) with CD4+ T lymphocytes is well studied and typically results in virally induced cytolysis. In contrast, relatively little is known concerning the interplay between HIV-1 and microglia. Recent findings suggest that, counter-intuitively, HIV-1 infection may extend the lifespan of microglia. We developed a novel cell line model system to confirm and mechanistically study this phenomenon. We found that transduction of a human microglial cell line with an HIV-1 vector results in a powerful cytoprotective effect following apoptotic challenge. This effect was reproduced by ectopic expression of a single virus-encoded protein, Tat. Subsequent studies showed that the pro-survival effects of intracellular Tat could be attributed to activation of the PI-3-kinase (PI3K)/Akt pathway in the microglial cell line. Furthermore, we found that expression of Tat led to decreased expression of PTEN, a negative regulator of the PI-3-K pathway. Consistent with this, decreased p53 activity and increased E2F activity were observed. Based on these findings, a model of possible regulatory circuits that intracellular Tat and HIV-1 infection engage during the cytoprotective event in microglia has been suggested. We propose that the expression of Tat may enable HIV-1 infected microglia to survive throughout the course of infection, leading to persistent HIV-1 production and infection in the central nervous system.
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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.