ArticleFrontiers in immunology2023
Zika virus modulates mitochondrial dynamics, mitophagy, and mitochondria-derived vesicles to facilitate viral replication in trophoblast cells.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 41 citations in OpenAlex.
- The oxidative stress paradigm in arbovirus infections: mechanisms and therapeutic insights.Redox report : communications in free radical research · 2026Review
- 3C suppresses PINK1-mediated mitophagy and contributes to coxsackievirus B3 replication.Virulence · 2026Article
- AMPK-Orchestrated Metabolic Reprogramming in Some Flavivirus Infections: Mechanisms and Therapeutic Opportunities.Viruses · 2026Review
- Review
- Coronavirus infectious bronchitis virus spike protein inhibits FUNDC1-mediated mitophagy to prevent nucleocapsid protein degradation.Journal of virology · 2026Article
- Protein NS4A of ZIKV Inhibits Glycolytic Flux by Targeting Enolase-1.Current issues in molecular biology · 2026Article
- Newcastle disease virus hijacks mitophagy to reprogram amino acid metabolism for enhanced replication.Autophagy · 2026Article
- Zika virus: unraveling the complex interplay between viral pathogenesis and host immune defenses.Virology journal · 2026Review
- A genus-wide interaction atlas across NS4B orthologues identifies a conserved role for UFMylation in orthoflavivirus replication.Nature communications · 2026Article
- Rewiring of host cell signaling in chikungunya virus infection: a mechanism for pathogenesis and therapeutic approaches.Archives of microbiology · 2026Review
- Zika Virus Reprograms Microglial Mitochondrial Metabolism to Support Immune Activation and Viral Replication: Omega-3 DHA Counteracts Neuroinflammation and Viral Persistence.Molecular neurobiology · 2026Article
- Zika virus and host innate immunity: mechanisms of activation and evasion.Frontiers in immunology · 2026Review
- Vertical Transmission of Zika Virus: The Immune-Pathophysiological Interface of the Placenta.Journal of immunology research · 2026Review
- Zika virus infection induces ultrastructural alterations, mitochondrial dysfunction and oxidative stress in human trophoblast HTR-8/SVneo.Frontiers in cellular and infection microbiology · 2026Article
- Mitochondrial quality control: a new mechanism for antiviral therapy.Frontiers in immunology · 2026Review
- BVDV utilizes PGC-1α downregulation to remodel the mitochondrial metabolic microenvironment, enhancing viral replication and impairing host immunity.Frontiers in veterinary science · 2026Article
- Comparison of human cerebral organoids infected with wild-type Zika versus attenuated DN-2 virus strains uncovers differences in host immune responses.Cell communication and signaling : CCS · 2025Article
- Comparative interactome analysis of Chikungunya virus non-structural protein 2 (CHIKV-nsP2) in human (Huh7) andVirusdisease · 2025Article
- Metabolic Reprogramming in Respiratory Viral Infections: A Focus on SARS-CoV-2, Influenza, and Respiratory Syncytial Virus.Biomolecules · 2025Review
- Understanding the mechanisms of mitochondrial rewiring during viral infections.The Journal of general virology · 2025Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zika virus (ZIKV) remains a global public health threat with the potential risk of a future outbreak. Since viral infections are known to exploit mitochondria-mediated cellular processes, we investigated the effects of ZIKV infection in trophoblast cells in terms of the different mitochondrial quality control pathways that govern mitochondrial integrity and function. Here we demonstrate that ZIKV (PRVABC59) infection of JEG-3 trophoblast cells manipulates mitochondrial dynamics, mitophagy, and formation of mitochondria-derived vesicles (MDVs). Specifically, ZIKV nonstructural protein 4A (NS4A) translocates to the mitochondria, triggers mitochondrial fission and mitophagy, and suppresses mitochondrial associated antiviral protein (MAVS)-mediated type I interferon (IFN) response. Furthermore, proteomics profiling of small extracellular vesicles (sEVs) revealed an enrichment of mitochondrial proteins in sEVs secreted by ZIKV-infected JEG-3 cells, suggesting that MDV formation may also be another mitochondrial quality control mechanism manipulated during placental ZIKV infection. Altogether, our findings highlight the different mitochondrial quality control mechanisms manipulated by ZIKV during infection of placental cells as host immune evasion mechanisms utilized by ZIKV at the placenta to suppress the host antiviral response and facilitate viral infection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.