HIV TAT-mediated microglial senescence: Role of SIRT3-dependent mitochondrial oxidative stress
Open accessAbstract
The advent of combined antiretroviral treatment (cART) as a treatment for HIV-1 infection has not only resulted in a dramatic decrease in the peripheral viral load but has also led to increased life expectancy of the infected individuals. Paradoxically, increased lifespan is accompanied with higher prevalence of age-related comorbidities, including HIV-associated neurocognitive disorders (HAND). Present study was aimed at exploring the role of HIV TAT protein in mediating microglial mitochondrial oxidative stress, ultimately resulting in neuroinflammation and microglial senescence. Our findings demonstrated that exposure of mouse primary microglial cells (mPMs) to HIV TAT protein resulted in a senescence-like phenotype, that was characterized by elevated expression of both p16 and p21 proteins, increased numbers of senescence-associated-β-galactosidase positive cells, augmented cell-cycle arrest, increased release of proinflammatory cytokines and decreased telomerase activity. Additionally, exposure of mPMs to HIV TAT also resulted downregulation of SIRT3 with a concomitant increase in mitochondrial oxidative stress. Dual luciferase reporter assay identified miR-505 as a novel target of SIRT3, which was upregulated in mPMs exposed to HIV TAT. Furthermore, transient transfection of mPMs with either the SIRT3 plasmid or miRNA-505 inhibitor upregulated the expression of SIRT3 and mitochondrial antioxidant enzymes, with a concomitant decrease in microglial senescence. These in vitro findings were also validated in the prefrontal cortices and striatum of HIV transgenic rats as well as cART-treated HIV-infected individuals. In summary, this study underscores a yet undiscovered novel mechanism(s) underlying HIV TAT-mediated induction of senescence phenotype in microglia, involving the miR-505-SIRT3 axis-mediated induction of mitochondrial oxidative stress.
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SIRT3 is downregulated in prefrontal cortex of HIV patients, along with upregulation of p16 and p21.
“This process is likely to be mediated by a Tat‐dependent downregulation of SIRT3, as the enzyme is found to be downregulated in the prefrontal cortex of HIV patients, along with an upregulation of p16 and p21 (Thangaraj et al, 2021).”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Thangaraj et al, 2021
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SIRT2 is required for lipopolysaccharide-induced activation of BV2 microglia
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Self-citationNeuroinflammation and Behavior in HIV-1 Transgenic Rats Exposed to Chronic Adolescent Stress
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HIV-1 Tat and Cocaine Impair Survival of Cultured Primary Neuronal Cells via a Mitochondrial Pathway
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NRF2 Antagonizes HIV-1 Tat and Methamphetamine-Induced BV2 Cell Ferroptosis by Regulating SLC7A11
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Sirtuins Modulation: A Promising Strategy for HIV-Associated Neurocognitive Impairments
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Sirtuins as Interesting Players in the Course of HIV Infection and Comorbidities
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Exploring viral neuropathic pain: Molecular mechanisms and therapeutic implications
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Self-citationAdvances in the Experimental Models of HIV-Associated Neurological Disorders
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Self-citationRole of SIRT3 in neurological diseases and rehabilitation training
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Role of Dysregulated Autophagy in HIV Tat, Cocaine, and cART Mediated NLRP3 Activation in Microglia
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Self-citationThe impacts of chronic infections on shaping cellular senescence
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The Epigenetic Role of miR-124 in HIV-1 Tat- and Cocaine-Mediated Microglial Activation
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Self-citationInfectious viruses and neurodegenerative diseases: The mitochondrial defect hypothesis
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HIV-Tat upregulates the expression of senescence biomarkers in CD4+ T-cells
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Epigenetics and Mitochondrial Biogenesis: The Role of Sirtuins in HIV Neuropathogenesis
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Emerging roles of senolytics/senomorphics in HIV-related co-morbidities
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Self-citationPathogenesis of HIV-associated depression: contributing factors and underlying mechanisms
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SLC38A9 is directly involved in Tat-induced endolysosome dysfunction and senescence in astrocytes
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Decoding miRNA-Mediated Immunoregulation in SARS-CoV-2, HBV, HIV, and HSV Infections
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TLR7 Mediates HIV ‐1 Tat‐Induced Cellular Senescence in Human Astrocytes
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HIV-1 Tat and gp120 as key drivers of neurodegeneration in the central nervous system
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PON-1 and PON-2 Polymorphisms and PON-1 Paraoxonase Activity in People Living with HIV-1
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- Authors
- Thangaraj, A., Chivero, E. T., Tripathi, A., Singh, S., Niu, F., Guo, M.-L., Pillai, P., Periyasamy, P., & Buch, S.
- Affiliations
- Nebraska Medical Center (US)
- Maharaja Sayajirao University of Baroda (IN)
- Corresponding author
- Buch, Shilpa
- ORCID
- Venue
- Redox Biology
- Publisher
- Elsevier BV
- Published
- 2021-04
- Volume
- 40
- Pages
- 101843
- ISSN
- 2213-2317 (ISSN-L)
- PMC
- PMC7779826
- OpenAlex
- W3115196011
- Cited by
- 76
- References
- 123
- Citations by year
- 2026: 14 · 2025: 16 · 2024: 14 · 2023: 16 · 2022: 7 · 2021: 9
- FWCI
- 4.21
- Type
- journal article
- Language
- en
- Update notices
- erratum (2021-08-01)
- Open access
- gold
- doi.org
- Licence
- Locations
- Redox Biology (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Drug Abuse
- National Institute of Mental Health
- Topics
- Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- HIV-1 Tat protein, microglial senescence, SIRT3, mitochondrial oxidative stress, miR-505, HIV-associated neurocognitive disorders, neuroinflammation, telomerase activity, highly active antiretroviral therapy
- MeSH terms
- Animals, HIV Infections, Microglia, Oxidative Stress, Mice, Rats, tat Gene Products, Human Immunodeficiency Virus, Sirtuin 3
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