ArticlePLoS pathogens2020
Zika virus infects pericytes in the choroid plexus and enters the central nervous system through the blood-cerebrospinal fluid barrier.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 77 citations in OpenAlex.
- Low-replication influenza virus mediates high pathogenicity through an inflammation-driven lung-heart-brain axis in mice.Emerging microbes & infections · 2026Article
- Brain defence by the extracellular matrix protein Cochlin.Communications biology · 2026Article
- Arboviral infections of the central nervous system: Mechanisms of invasion and long-term consequences.Journal of neurovirology · 2026Review
- Article
- The Forgotten Gate: Choroid Plexus and Blood-CSF Barrier in Arboviral Encephalitis.Life (Basel, Switzerland) · 2026Review
- Breaking barriers and beyond: Mechanisms and pathological implications of Zika virus traversal across blood-tissue interfaces.Virologica Sinica · 2026Review
- Discovery of a potent anti-Zika virus benzamide series targeting the viral protein NS4B.PLoS pathogens · 2026Article
- A case-control neuroimaging investigation of chronic Zika virus-infected adults.Frontiers in human neuroscience · 2026Article
- Discovery of a potent anti-Zika virus benzamide series targeting the viral protein NS4B.bioRxiv : the preprint server for biology · 2025Article
- Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025Review
- Neurovascular pericytes are susceptible to infection by JC polyomavirus.Journal of virology · 2025Article
- Role of non-human primate models in accelerating research and developing countermeasures against Zika virus infection.The Lancet. Microbe · 2025Review
- Cognitive Sequelae of COVID-19: Mechanistic Insights and Therapeutic Approaches.CNS neuroscience & therapeutics · 2025Review
- Viruses and the Brain-A Relationship Prone to Trouble.Viruses · 2025Review
- Congenital Zika virus infection in laboratory animals: a comparative review highlights translational studies on the maternal-foetal interface.Memorias do Instituto Oswaldo Cruz · 2025Review
- Neural and endothelial cell-derived extracellular vesicles mediate Zika virus genome dissemination and productive infection in vivo.PloS one · 2025Article
- Distinct ZIKV strain signatures and type I IFN modulation reveal a protective role of brain endothelial interferon signalingFrontiers in cellular and infection microbiology · 2025Article
- EV-A71 invades the central nervous system and affects the blood-brain barrier in a tree shrew model.Frontiers in immunology · 2025Article
- VLDLR mediates Semliki Forest virus neuroinvasion through the blood-cerebrospinal fluid barrier.Nature communications · 2024Article
- Knowns and unknowns of TiLV-associated neuronal disease.Virulence · 2024Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zika virus (ZIKV) can infect and cause microcephaly and Zika-associated neurological complications in the developing fetal and adult brains. In terms of pathogenesis, a critical question is how ZIKV overcomes the barriers separating the brain from the circulation and gains access to the central nervous system (CNS). Despite the importance of ZIKV pathogenesis, the route ZIKV utilizes to cross CNS barriers remains unclear. Here we show that in mouse models, ZIKV-infected cells initially appeared in the periventricular regions of the brain, including the choroid plexus and the meninges, prior to infection of the cortex. The appearance of ZIKV in cerebrospinal fluid (CSF) preceded infection of the brain parenchyma. Further the brain infection was significantly attenuated by neutralization of the virus in the CSF, indicating that ZIKV in the CSF at the early stage of infection might be responsible for establishing a lethal infection of the brain. We show that cells infected by ZIKV in the choroid plexus were pericytes. Using in vitro systems, we highlight the possibility that ZIKV crosses the blood-CSF barrier by disrupting the choroid plexus epithelial layer. Taken together, our results suggest that ZIKV might exploit the blood-CSF barrier rather than the blood-brain barrier to invade the CNS.
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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.