ArticleJournal of neuroinflammation2022
SARS-CoV-2 productively infects human brain microvascular endothelial cells.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- Posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome in patients with COVID-19 infection: is there a link? A systematic review and case report analysis.Journal of neurology · 2023Pooled it
- SARS-CoV-2 disrupts the integrity of a human blood-brain barrier model in the absence of infection.Journal of neurovirology · 2026Article
- COVID-19 Is Airborne AIDS: Provocative Oversimplification, Emerging Science, or Something in Between?AJPM focus · 2026Review
- Blood-Brain Barrier Changes and Related Microvascular Outcomes in Long-COVID: A Comprehensive Review.Life (Basel, Switzerland) · 2026Review
- Review
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- Human coronavirus OC43 infection in human cerebral organoids: novel insights on pathogenesis and potential therapeutic interventions.Journal of biomedical science · 2025Article
- A survey of SARS-CoV-2 tropism.Infectious diseases & immunity · 2025Review
- Sustained Vascular Inflammatory Effects of SARS-CoV-2 Spike Protein on Human Endothelial Cells.Inflammation · 2025Article
- SARS-Cov-2 Replication in a Blood-Brain Barrier Model Established with Human Brain Microvascular Endothelial Cells Induces Permeability and Disables ACE2-Dependent Regulation of Bradykinin B1 Receptor.International journal of molecular sciences · 2025Article
- The Molecular Mechanisms of Cognitive Dysfunction in Long COVID: A Narrative Review.International journal of molecular sciences · 2025Review
- Article
- Innate immune sensors and regulators at the blood brain barrier: focus on toll-like receptors and inflammasomes as mediators of neuro-immune crosstalk and inflammation.Journal of neuroinflammation · 2025Review
- Cerebromicrovascular mechanisms contributing to long COVID: implications for neurocognitive health.GeroScience · 2025Review
- A vascular endothelial cell, neuron, and microglia tri-culture model to study hypertension-related depression.Frontiers in cellular neuroscience · 2025Article
- Cardiovascular damage and comorbidities related to long COVID: pathomechanisms, prevention, and therapy.Frontiers in cardiovascular medicine · 2025Review
- Cognition-associated gray matter volume alterations in long-COVID show sex-specific patterns.Frontiers in psychiatry · 2025Article
- A data-mining analysis of host solute carrier family proteins in SARS-CoV-2 infection with reference to brain endothelial cells and the blood-brain barrier in COVID-19.Frontiers in neurology · 2025Article
- Infections withFrontiers in aging neuroscience · 2025Review
- Virally-initiated pain states: phenotypes, mechanisms, and future directions.Frontiers in pain research (Lausanne, Switzerland) · 2025Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe emergence of the novel, pathogenic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a global health emergency. SARS-CoV-2 is highly contagious and has a high mortality rate in severe patients. However, there is very limited information on the effect of SARS-CoV-2 infection on the integrity of the blood-brain barrier (BBB).
methodsRNA-sequencing profiling was performed to analyze the transcriptomic changes in human brain microvascular endothelial cells (hBMECs) after SARS-CoV-2 infection. Bioinformatic tools were used for differential analysis. Immunofluorescence, real-time quantitative PCR, and Western blotting analysis were used to explore biological phenotypes.
resultsA total of 927 differentially expressed genes were identified, 610 of which were significantly upregulated while the remaining 317 were downregulated. We verified the significant induction of cytokines, chemokines, and adhesion molecules in hBMECs by SARS-CoV-2, suggesting an activation of the vascular endothelium in brain. Moreover, we demonstrated that SARS-CoV-2 infection could increase the BBB permeability, by downregulating as well as remodeling the intercellular tight junction proteins.
conclusionsOur findings demonstrated that SARS-CoV-2 infection can cause BBB dysfunction, providing novel insights into the understanding of SARS-CoV-2 neuropathogenesis. Moreover, this finding shall constitute a new approach for future prevention and treatment of SARS-CoV-2-induced CNS infection.
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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.