ArticlePLoS pathogens2023
Ebola virus disrupts the inner blood-retinal barrier by induction of vascular endothelial growth factor in pericytes.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Ebola Virus Persistence Beyond Acute Infection: Could HIV-Associated Immune Dysfunction Influence Survivor Biology?Viruses · 2026Review
- Ponatinib and other clinically approved inhibitors of Src and Rho-A kinases abrogate dengue virus serotype 2- induced endothelial permeability.Virulence · 2025Article
- Ebola's hidden front: Neurological involvement and pathogenesis.PLoS pathogens · 2025Article
- Filovirus infection disrupts epithelial barrier function and ion transport in human iPSC-derived gut organoids.PLoS pathogens · 2025Article
- Ebola virus' hidden target: virus transmission to and infection of skin.Journal of virology · 2025Article
- Ocular neuroinflammatory response secondary to SARS-CoV-2 infection-a review.Frontiers in immunology · 2025Review
- Hippo signaling pathway regulates Ebola virus transcription and egress.Nature communications · 2024Article
- SARS-CoV-2 infects cells lining the blood-retinal barrier and induces a hyperinflammatory immune response in the retina via systemic exposure.PLoS pathogens · 2024Article
- Contrasting effects of filamin A and B proteins in modulating filovirus entry.PLoS pathogens · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ebola virus (EBOV) causes severe hemorrhagic fever in humans with high mortality. In Ebola virus disease (EVD) survivors, EBOV persistence in the eyes may break through the inner blood-retinal barrier (iBRB), leading to ocular complications and EVD recurrence. However, the mechanism by which EBOV affects the iBRB remains unclear. Here, we used the in vitro iBRB model to simulate EBOV in retinal tissue and found that Ebola virus-like particles (EBO-VLPs) could disrupt the iBRB. Cytokine screening revealed that EBO-VLPs stimulate pericytes to secrete vascular endothelial growth factor (VEGF) to cause iBRB breakdown. VEGF downregulates claudin-1 to disrupt the iBRB. Ebola glycoprotein is crucial for VEGF stimulation and iBRB breakdown. Furthermore, EBO-VLPs caused iBRB breakdown by stimulating VEGF in rats. This study provides a mechanistic insight into that EBOV disrupts the iBRB, which will assist in developing new strategies to treat EBOV persistence in EVD survivors.
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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.