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Induction of a Senescence-Like Phenotype in Cultured Human Fetal Microglia During HIV-1 Infection
Journal article   Open access   Peer reviewed

Induction of a Senescence-Like Phenotype in Cultured Human Fetal Microglia During HIV-1 Infection

Natalie C. Chen, Andrea T. Partridge, Ferit Tuzer, Justin Cohen, Timothy Nacarelli, Sonia Navas-Martin, Christian Sell, Claudio Torres and Julio Martin-Garcia
The journals of gerontology. Series A, Biological sciences and medical sciences, v 73(9), pp 1187-1196
01 Sep 2018
PMID: 29415134
url
https://doi.org/10.1093/gerona/gly022View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open

Abstract

Geriatrics & Gerontology Gerontology Life Sciences & Biomedicine Science & Technology
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 beta-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 naive 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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Web of Science research areas
Geriatrics & Gerontology
Gerontology
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