ArticleActa neuropathologica communications2017
Zika virus tropism and interactions in myelinating neural cell cultures: CNS cells and myelin are preferentially affected.
Article in Acta neuropathologica communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Guillain-Barré syndrome related to Zika virus infection: A systematic review and meta-analysis of the clinical and electrophysiological phenotype.PLoS neglected tropical diseases · 2020Pooled it
- From Perinatal Stress to Schizophrenia: The Emerging Role of Glial Pathology.Annals of neurosciences · 2026Review
- Chronic Neuroplasticity Changes Following Neurotropic Viral Infection: Mechanisms and Implications.Cellular and molecular neurobiology · 2025Review
- Peripheral nerve injury mediated by JEV strain NX1889 infection and impairment of Schwann cells.PLoS neglected tropical diseases · 2025Article
- The human neural cell atlas of Zika virus infection in developing brain tissue.Cell reports. Medicine · 2025Article
- Inflammation's impact on the interaction between oligodendrocytes and axons.Discovery immunology · 2025Review
- Translocator protein (TSPO) is a biomarker of Zika virus (ZIKV) infection-associated neuroinflammation.Emerging microbes & infections · 2024Article
- Zika Virus Neuropathogenesis-Research and Understanding.Pathogens (Basel, Switzerland) · 2024Review
- Disruption of myelin structure and oligodendrocyte maturation in a macaque model of congenital Zika infection.Nature communications · 2024Article
- Article
- Molecular and Cellular Mechanisms Underlying Neurologic Manifestations of Mosquito-Borne Flavivirus Infections.Viruses · 2023Review
- Pathophysiology and mechanisms of hearing impairment related to neonatal infection diseases.Frontiers in microbiology · 2023Review
- SARM1 detection in myelinating glia:Frontiers in cellular neuroscience · 2023Article
- Myelinating Co-Culture as a Model to Study Anti-NMDAR Neurotoxicity.International journal of molecular sciences · 2022Article
- Mucosal Responses to Zika Virus Infection in Cynomolgus Macaques.Pathogens (Basel, Switzerland) · 2022Article
- Article
- Perivascular Mesenchymal Stem/Stromal Cells, an Immune Privileged Niche for Viruses?International journal of molecular sciences · 2022Review
- Article
- Zika virus vertical transmission in interferon receptor1-antagonized Rag1Acta neuropathologica communications · 2022Article
- SARM1 Depletion Slows Axon Degeneration in a CNS Model of Neurotropic Viral Infection.Frontiers in molecular neuroscience · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
The recent global outbreak of Zika virus (ZIKV) infection has been linked to severe neurological disorders affecting the peripheral and central nervous systems (PNS and CNS, respectively). The pathobiology underlying these diverse clinical phenotypes are the subject of intense research; however, even the principal neural cell types vulnerable to productive Zika infection remain poorly characterised. Here we used CNS and PNS myelinating cultures from wild type and Ifnar1 knockout mice to examine neuronal and glial tropism and short-term consequences of direct infection with a Brazilian variant of ZIKV. Cell cultures were infected pre- or post-myelination for various intervals, then stained with cell-type and ZIKV-specific antibodies. In bypassing systemic immunity using ex vivo culture, and the type I interferon response in Ifnar1 deficient cells, we were able to evaluate the intrinsic infectivity of neural cells. Through systematic quantification of ZIKV infected cells in myelinating cultures, we found that ZIKV infection is enhanced in the absence of the type I interferon responses and that CNS cells are considerably more susceptible to infection than PNS cells. In particular, we demonstrate that CNS axons and myelinating oligodendrocytes are especially vulnerable to injury. These results have implications for understanding the pathobiology of neurological symptoms associated with ZIKV infection. Furthermore, we provide a quantifiable ex vivo infection model that can be used for fundamental and therapeutic studies on viral neuroinvasion and its consequences.
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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.