ArticlePloS one2014
Enterovirus 71 induces mitochondrial reactive oxygen species generation that is required for efficient replication.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 89 citations in OpenAlex.
- Roles of Reactive Oxygen Species in Relationships Between Viral Infections and Alzheimer's Disease and Related Dementia.Antioxidants (Basel, Switzerland) · 2026Review
- Transcriptome Analysis Reveals Gemykibivirus Infection Induces Mitochondrial DNA Release in HEK293T Cells.Viruses · 2025Article
- Flavonoids from Polygonum hydropiper L. regulate PCV2-induced oxidative stress of RAW264.7 cells via Pi3k/AKT and Nrf2/HO-1 signaling pathways.Scientific reports · 2025Article
- Metabolic Imprint of Poliovirus on Glioblastoma Cells and Its Role in Virus Replication and Cytopathic Activity.International journal of molecular sciences · 2025Article
- The structural protein VP3 of enterovirus D68 interacts with MAVS to inhibit the NF-κB signaling pathway.Journal of virology · 2025Article
- Effects of oxidative stress on viral infections: an overview.Npj viruses · 2025Review
- Viruses and psychiatric disorders: We have not crossed the borderline from hypothesis to proof yet (Review).Molecular medicine reports · 2025Review
- Insight into the Life Cycle of Enterovirus-A71.Viruses · 2025Review
- AVL-armed oncolytic vaccinia virus promotes viral replication and boosts antitumor immunity via increasing ROS levels in pancreatic cancer.Molecular therapy. Oncology · 2024Article
- Common Chemical Plasticizer Di(2-Ethhylhexyl) Phthalate Exposure Exacerbates Coxsackievirus B3 Infection.Viruses · 2024Article
- Metabolomics combined with network pharmacology reveals a role for astragaloside IV in inhibiting enterovirus 71 replication via PI3K-AKT signaling.Journal of translational medicine · 2024Article
- Mitochondrial Reactive Oxygen Species in Infection and Immunity.Biomolecules · 2024Review
- Leucoverdazyls as Novel Potent Inhibitors of Enterovirus Replication.Pathogens (Basel, Switzerland) · 2024Article
- Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection.Molecular neurobiology · 2024Review
- Talk to Me-Interplay between Mitochondria and Microbiota in Aging.International journal of molecular sciences · 2023Review
- Article
- Carbon-based nanomaterials against SARS-CoV-2: Therapeutic and diagnostic applications.OpenNano · 2023Article
- Malonyl-CoA Accumulation as a Compensatory Cytoprotective Mechanism in Cardiac Cells in Response to 7-Ketocholesterol-Induced Growth Retardation.International journal of molecular sciences · 2023Article
- Enteroviral 2B Interacts with VDAC3 to Regulate Reactive Oxygen Species Generation That Is Essential to Viral Replication.Viruses · 2022Article
- Nanomaterials and metal-organic frameworks for biosensing applications of mutations of the emerging viruses.Analytical biochemistry · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Redox homeostasis is an important host factor determining the outcome of infectious disease. Enterovirus 71 (EV71) infection has become an important endemic disease in Southeast Asia and China. We have previously shown that oxidative stress promotes viral replication, and progeny virus induces oxidative stress in host cells. The detailed mechanism for reactive oxygen species (ROS) generation in infected cells remains elusive. In the current study, we demonstrate that mitochondria were a major ROS source in EV71-infected cells. Mitochondria in productively infected cells underwent morphologic changes and exhibited functional anomalies, such as a decrease in mitochondrial electrochemical potential ΔΨ(m) and an increase in oligomycin-insensitive oxygen consumption. Respiratory control ratio of mitochondria from infected cells was significantly lower than that of normal cells. The total adenine nucleotide pool and ATP content of EV71-infected cells significantly diminished. However, there appeared to be a compensatory increase in mitochondrial mass. Treatment with mito-TEMPO reduced eIF2α phosphorylation and viral replication, suggesting that mitochondrial ROS act to promote viral replication. It is plausible that EV71 infection induces mitochondrial ROS generation, which is essential to viral replication, at the sacrifice of efficient energy production, and that infected cells up-regulate biogenesis of mitochondria to compensate for their functional defect.
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