ArticleGlia2021
Oligodendrocytes are susceptible to Zika virus infection in a mouse model of perinatal exposure: Implications for CNS complications.
Article in Glia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 42 citations in OpenAlex.
- Beyond the neuron: the role of glial cells in viral neuropathogenesis.Journal of virology · 2026Review
- A case-control neuroimaging investigation of chronic Zika virus-infected adults.Frontiers in human neuroscience · 2026Article
- Role of innate immune and inflammatory signaling in West Nile virus tropism and neuronal and glial cell death.Scientific reports · 2025Article
- Viruses and the Brain-A Relationship Prone to Trouble.Viruses · 2025Review
- Inflammation's impact on the interaction between oligodendrocytes and axons.Discovery immunology · 2025Review
- Epidemic Zika virus strains from the Asian lineage induce an attenuated fetal brain pathogenicity.Nature communications · 2024Article
- Translocator protein (TSPO) is a biomarker of Zika virus (ZIKV) infection-associated neuroinflammation.Emerging microbes & infections · 2024Article
- Human Brain In Vitro Model for Pathogen Infection-Related Neurodegeneration Study.International journal of molecular sciences · 2024Review
- Oligodendrocyte-derived IL-33 functions as a microglial survival factor during neuroinvasive flavivirus infection.PLoS pathogens · 2023Article
- Molecular and Cellular Mechanisms Underlying Neurologic Manifestations of Mosquito-Borne Flavivirus Infections.Viruses · 2023Review
- Review
- Organotypic hippocampal culture model reveals differential responses to highly similar Zika virus isolates.Journal of neuroinflammation · 2023Article
- Review
- Mechanisms of Zika astrocyte infection and neuronal toxicity.NeuroImmune pharmacology and therapeutics · 2023Article
- Modeling infectious diseases of the central nervous system with human brain organoids.Translational research : the journal of laboratory and clinical medicine · 2022Review
- Apoptosis during ZIKA Virus Infection: Too Soon or Too Late?International journal of molecular sciences · 2022Review
- The legacy of ZikaPLAN: a transnational research consortium addressing Zika.Global health action · 2021Review
- Article
- Acute neurologic emerging flaviviruses.Therapeutic advances in infectious diseaseReview
- Inflammation Unleashed in Viral-Induced Epileptogenesis.Epilepsy currentsArticle
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Some children with proven intrauterine Zika virus (ZIKV) infection who were born asymptomatic subsequently manifested neurodevelopmental delays, pointing to impairment of development perinatally and postnatally. To model this, we infected postnatal day (P) 5-6 (equivalent to the perinatal period in humans) susceptible mice with a mammalian cell-propagated ZIKV clinical isolate from the Brazilian outbreak in 2015. All infected mice appeared normal up to 4 days post-intraperitoneal inoculation (dpi), but rapidly developed severe clinical signs at 5-6 dpi. All nervous tissue examined at 5/6 dpi appeared grossly normal. However, anti-ZIKV positive cells were observed in the optic nerve, brain, and spinal cord; predominantly in white matter. Co-labeling with cell type specific markers demonstrated oligodendrocytes and astrocytes support productive infection. Rarely, ZIKV positive neurons were observed. In spinal cord white matter, which we examined in detail, apoptotic cells were evident; the density of oligodendrocytes was significantly reduced; and there was localized microglial reactivity including expression of the NLRP3 inflammasome. Together, our observations demonstrate that a clinically relevant ZIKV isolate can directly impact oligodendrocytes. As primary oligodendrocyte cell death can lead later to secondary autoimmune demyelination, our observations may help explain neurodevelopmental delays in infants appearing asymptomatic at birth and commend lifetime surveillance.
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Registered trials
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.