ArticleScientific reports2020
Zika virus infection leads to mitochondrial failure, oxidative stress and DNA damage in human iPSC-derived astrocytes.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 143 citations in OpenAlex.
- The oxidative stress paradigm in arbovirus infections: mechanisms and therapeutic insights.Redox report : communications in free radical research · 2026Review
- Beyond the neuron: the role of glial cells in viral neuropathogenesis.Journal of virology · 2026Review
- Article
- Lipid peroxidation impacts orthoflavivirus infection in a virus-dependent manner.Cell death & disease · 2026Article
- Breaking barriers and beyond: Mechanisms and pathological implications of Zika virus traversal across blood-tissue interfaces.Virologica Sinica · 2026Review
- Impact of Selenium and Vitamin E Deficiency on Zika Virus Pathogenesis and Immune Response in Mice.Viruses · 2026Article
- Zika Virus Reprograms Microglial Mitochondrial Metabolism to Support Immune Activation and Viral Replication: Omega-3 DHA Counteracts Neuroinflammation and Viral Persistence.Molecular neurobiology · 2026Article
- A case-control neuroimaging investigation of chronic Zika virus-infected adults.Frontiers in human neuroscience · 2026Article
- Zika virus infection induces ultrastructural alterations, mitochondrial dysfunction and oxidative stress in human trophoblast HTR-8/SVneo.Frontiers in cellular and infection microbiology · 2026Article
- Zika Virus Infection Is More Highly Replicative and Transmissible by Extracellular Vesicles in Human than in Mouse Neuronal Cells.International journal of molecular sciences · 2025Article
- Zika virus impairs non-homologous end joining and exacerbates DNA damage in neural progenitors derived from Huntington's disease iPSCs via mutant huntingtin-elicited Ku70/Ku80 complex disruption.Stem cell research & therapy · 2025Article
- Metabolic characteristics in orthoflaviviral infections: unveiling pathogenic mechanisms and therapeutic targets.Virology journal · 2025Review
- Understanding the mechanisms of mitochondrial rewiring during viral infections.The Journal of general virology · 2025Review
- Unveiling the cardiovascular impact of Zika Virus: Myocardial injury, prothrombotic state, and oxidative stress in immunocompetent mice.PLoS neglected tropical diseases · 2025Article
- Circadian misalignment potentiates blood-brain barrier disruption and mitochondria dysregulation in Zika virus infection.Fluids and barriers of the CNS · 2025Article
- New perspectives on heterogeneity in astrocyte reactivity in neuroinflammation.Brain, behavior, & immunity - health · 2025Article
- High glucose potentiates Zika virus induced-astroglial dysfunctions.Journal of neurovirology · 2025Article
- Genotoxic consequences of viral infections.Npj viruses · 2025Review
- Glutamine-glutamate centered metabolism as the potential therapeutic target against Japanese encephalitis virus-induced encephalitis.Cell & bioscience · 2025Article
- Dengue virus and Zika virus alter endoplasmic reticulum-mitochondria contact sites to regulate respiration and apoptosis.iScience · 2025Article
33 more citing papers are in PubMed but not listed here.
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Authors and funding
25 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zika virus (ZIKV) has been extensively studied since it was linked to congenital malformations, and recent research has revealed that astrocytes are targets of ZIKV. However, the consequences of ZIKV infection, especially to this cell type, remain largely unknown, particularly considering integrative studies aiming to understand the crosstalk among key cellular mechanisms and fates involved in the neurotoxicity of the virus. Here, the consequences of ZIKV infection in iPSC-derived astrocytes are presented. Our results show ROS imbalance, mitochondrial defects and DNA breakage, which have been previously linked to neurological disorders. We have also detected glial reactivity, also present in mice and in post-mortem brains from infected neonates from the Northeast of Brazil. Given the role of glia in the developing brain, these findings may help to explain the observed effects in congenital Zika syndrome related to neuronal loss and motor deficit.
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