ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2018
Induction of a Senescence-Like Phenotype in Cultured Human Fetal Microglia During HIV-1 Infection.
Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Hypothalamic Inflammaging: A Central Driver of Type 2 Diabetes Mellitus and Metabolic Disease in Aging.Diabetes & metabolism journal · 2026Review
- Neuroinflammation and NeuroHIV: understanding the role of HIV-1 related factors in microglial activation.Translational psychiatry · 2026Review
- HIV infection in microglia leads to senescence, triggering activation of neurotoxicity pathways.bioRxiv : the preprint server for biology · 2025Article
- Age-associated microglial transcriptome leads to diminished immunogenicity and dysregulation of MCT4 and P2RY12/P2RY13 related functions.Cell death discovery · 2025Article
- HIV-Tat upregulates the expression of senescence biomarkers in CD4Frontiers in immunology · 2025Article
- HIV Protein Nef Induces Cardiomyopathy Through Induction of Bcl2 and p21.International journal of molecular sciences · 2024Article
- Article
- Talk to Me-Interplay between Mitochondria and Microbiota in Aging.International journal of molecular sciences · 2023Review
- Involvement of lncRNA TUG1 in HIV-1 Tat-Induced Astrocyte Senescence.International journal of molecular sciences · 2023Article
- Self-DNA driven inflammation in COVID-19 and after mRNA-based vaccination: lessons for non-COVID-19 pathologies.Frontiers in immunology · 2023Article
- Senotherapeutics in Cancer and HIV.Cells · 2022Review
- The struggle of a good friend getting old: cellular senescence in viral responses and therapy.EMBO reports · 2021Review
- Aged Microglia in Neurodegenerative Diseases: Microglia Lifespan and Culture Methods.Frontiers in aging neuroscience · 2021Review
- Brain aging and garbage cleaning : Modelling the role of sleep, glymphatic system, and microglia senescence in the propagation of inflammaging.Seminars in immunopathology · 2020Review
- Senotherapeutics and HIV-1 Persistence.Current HIV/AIDS reports · 2020Review
- Review
- Astrocyte senescence: Evidence and significance.Aging cell · 2019Review
- Article
- Old age increases microglial senescence, exacerbates secondary neuroinflammation, and worsens neurological outcomes after acute traumatic brain injury in mice.Neurobiology of aging · 2019Article
- Current and Future Therapeutic Strategies for Lentiviral Eradication from Macrophage Reservoirs.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
HIV-1 causes premature aging in chronically infected patients. Despite effective anti-retroviral therapy, around 50% of patients suffer HIV-associated neurocognitive disorders (HAND), which likely potentiate aging-associated neurocognitive decline. Microglia support productive HIV-1 infection in the brain. Elevated markers of cellular senescence, including p53 and p21, have been detected in brain tissues from patients with HAND, but the potential for microglia senescence during HIV-1 infection has not been investigated. We hypothesized that HIV-1 can induce senescence in microglia. Primary human fetal microglia were exposed to single-round infectious HIV-1 pseudotypes or controls, and examined for markers of senescence. Post-infection, microglia had significantly elevated: senescence-associated β-galactosidase activity, p21 levels, and production of cytokines such as IL-6 and IL-8, potentially indicative of a senescence-associated secretory phenotype. We also found increased detection of p53-binding protein foci in microglia nuclei post-infection. Additionally, we examined mitochondrial reactive oxygen species (ROS) and respiration, and found significantly increased mitochondrial ROS levels and decreased ATP-linked respiration during HIV-1 infection. Supernatant transfer from infected cultures to naïve microglia resulted in elevated p21 and caveolin-1 levels, and IL-8 production. Finally, nucleoside treatment reduced senescence markers induction in microglia. Overall, HIV-1 induces a senescence-like phenotype in human microglia, which could play a role 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 Socratic graph.