ArticleFrontiers in immunology2018
Cell Death Is Counteracted by Mitophagy in HIV-Productively Infected Astrocytes but Is Promoted by Inflammasome Activation Among Non-productively Infected Cells.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Human papillomavirus E7 inhibits immune responses in keratinocytes by activating HTRA1‑mediated mitophagy.International journal of molecular medicine · 2026Article
- SARS-CoV-2-Induced Macrophage Polarization Reverses HIV-1 Latency in J-Lat Cells Through TNFα Signaling.Journal of immunology research · 2026Article
- Astroglia-mediated neuroinflammation as a putative mechanism of neurological outcomes in COVID-19? Insights from a Brazilian cohort.Brain, behavior, & immunity - health · 2025Article
- Mitochondrial Dysfunction in Aging, HIV, and Long COVID: Mechanisms and Therapeutic Opportunities.Pathogens (Basel, Switzerland) · 2025Review
- Ferroptosis and mitochondrial ROS are central to SARS-CoV-2-induced hepatocyte death.Frontiers in cellular and infection microbiology · 2025Article
- Review
- Investigating the interplay between mitophagy and diabetic neuropathy: Uncovering the hidden secrets of the disease pathology.Pharmacological research · 2024Review
- Molecular mechanism and potential role of mitophagy in acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Mitochondrial Reactive Oxygen Species in Infection and Immunity.Biomolecules · 2024Review
- Review
- Review
- The NLRP3 inflammasome and gut dysbiosis as a putative link between HIV-1 infection and ischemic stroke.Trends in neurosciences · 2023Review
- HIV-1 activates oxidative phosphorylation in infected CD4 T cells in a human tonsil explant model.Frontiers in immunology · 2023Article
- Review
- The Role of Mitophagy in Viral Infection.Cells · 2022Review
- Using 2D and 3D pluripotent stem cell models to study neurotropic viruses.Frontiers in virology (Lausanne, Switzerland) · 2022Article
- A Non-Canonical Role for IRE1α Links ER and Mitochondria as Key Regulators of Astrocyte Dysfunction: Implications in Methamphetamine use and HIV-Associated Neurocognitive Disorders.Frontiers in neuroscience · 2022Article
- Mitochondria as a Cellular Hub in Infection and Inflammation.International journal of molecular sciences · 2021Review
- Oxidized mitochondrial DNA released after inflammasome activation is a disease biomarker for myelodysplastic syndromes.Blood advances · 2021Article
- Nilotinib Improves Bioenergetic Profiling in Brain Astroglia in the 3xTg Mouse Model of Alzheimer's Disease.Aging and disease · 2021Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite more than 30 years of extensive research efforts, a complete understanding of the neurological consequences of HIV central nervous system (CNS) infection remains elusive. HIV is not only able to establish a viral reservoir in the CNS but also to initiate manifestation of neurodegenerative diseases. These neurological disorders may arise because of virus-induced activation of the inflammasome in CNS cells, including astrocytes. Nevertheless, in some productive viral infection scenarios, selective autophagy may reduce inflammation through mitochondrial degradation ("mitophagy") to counteract inflammasome activation. In this study, using cultured human astrocytes, we demonstrate that-depending on the HIV infection outcome-cells may resist death, or succumb by inflammasome activation when viral infection is productive or abortive, respectively. Cells productively infected with HIV were able to attenuate both mitochondrial ROS production and mitochondrial membrane potential dissipation, thus exhibiting cell death resistance. Interestingly, mitochondrial injury was counteracted by increasing the autophagic flux and by activating mitophagy. Conversely, astrocytes exposed to HIV in an abortive scenario showed prominent mitochondrial damage, inflammasome activation, and cell death. This bystander effect occurred after cell-to-cell contact with HIV-productively infected astrocytes. In summary, we demonstrate a tight functional crosstalk between viral infection mode, inflammasome activation, autophagy pathways and cell fate in the context of HIV infection. Moreover, mitophagy is crucial for cell death resistance in HIV-productively infected astrocytes, but its impairment may favor inflammasome-mediated cell death in abortively infected cells.
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