ArticleViruses2021
Reactive Oxygen Species (ROS) Are Not a Key Determinant for Zika Virus-Induced Apoptosis in SH-SY5Y Neuroblastoma Cells.
Article in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Article
- Fatty acid transporter protein isoform 2 (FATP2) inhibitor lipofermata inhibits Zika virus replication and blocks fatty acid uptake in SH-SY5Y neuroblastoma cell line.Microbiology spectrum · 2026Article
- Roles of Reactive Oxygen Species in Relationships Between Viral Infections and Alzheimer's Disease and Related Dementia.Antioxidants (Basel, Switzerland) · 2026Review
- Effects of oxidative stress on viral infections: an overview.Npj viruses · 2025Review
- Zika Virus Infection Alters the Circadian Clock Expression in Human Neuronal Monolayer and Neurosphere Cultures.Cellular and molecular neurobiology · 2023Article
- Redox Regulation and Metabolic Dependency of Zika Virus Replication: Inhibition by Nrf2-Antioxidant Response and NAD(H) Antimetabolites.Journal of virology · 2023Article
- Integrated re-analysis of transcriptomic and proteomic datasets reveals potential mechanisms for Zika viral-based oncolytic therapy in neuroblastoma.F1000Research · 2023Article
- Chikungunya virus infection induces ultrastructural changes and impaired neuronal differentiation of human neurospheres.Frontiers in microbiology · 2023Article
- Apoptosis during ZIKA Virus Infection: Too Soon or Too Late?International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionZIKV is a highly neurotropic virus that can cause the death of infected neuroprogenitor cells through mitochondrial damage and intrinsic apoptotic signaling. In this context, the role of reactive oxygen species (ROS) in neuronal cell death caused by ZIKV still remains elusive.
objectiveWe aimed at evaluating the role of these cellular components in the death of human undifferentiated neuroblastoma cell line infected with ZIKV.
resultsZIKV infection resulted in the extensive death of SH-SY5Y cells with the upregulation of several genes involved in survival and apoptotic responses as well as the colocalization of mitochondrial staining with ZIKV Envelope (E) protein. Notably, levels of intracellular reactive oxygen species (ROS) were not altered during ZIKV infection in undifferentiated SH-SY5Y cells, and consistent with these results, the treatment of infected cells with the widely studied ROS scavenger N-acetylcysteine (NAC) did not prevent cell death in these cells.
conclusionAltogether, our results suggest that excessive ROS production is not the main trigger of SH-SY5Y cells death in ZIKV infection.
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