ArticleJournal of neurovirology2019
Proteomics analysis of HSV-1-induced alterations in mouse brain microvascular endothelial cells.
Article in Journal of neurovirology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Serotype-specific host proteome remodeling in human foreskin fibroblasts during lytic HSV-1 and HSV-2 infection.Virology journal · 2025Article
- A microengineered 3D human neurovascular unit model to probe the neuropathogenesis of herpes simplex encephalitis.Nature communications · 2025Article
- 4D-DIA-Based Quantitative Proteomic Analysis Reveals the Involvement of TRPV2 Protein in Duck Tembusu Virus Replication.Viruses · 2024Article
- SUN2 Modulates the Propagation of HSV-1.Journal of virology · 2022Article
- Omics of endothelial cell dysfunction in sepsis.Vascular biology (Bristol, England) · 2022Review
- Gene Ontology curation of the blood-brain barrier to improve the analysis of Alzheimer's and other neurological diseases.Database : the journal of biological databases and curation · 2021Article
- Asymptomatic Herpes Simplex Virus Type 1 Infection Causes an Earlier Onset and More Severe Experimental Autoimmune Encephalomyelitis.Frontiers in immunology · 2021Article
- Interrogating Host Antiviral Environments Driven by Nuclear DNA Sensing: A Multiomic Perspective.Biomolecules · 2020Review
- Review
- Herpes Simplex Virus 1-Induced Blood-Brain Barrier Damage Involves Apoptosis Associated With GM130-Mediated Golgi Stress.Frontiers in molecular neuroscience · 2020Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus 1 (HSV-1) is a predominant cause of herpes simplex encephalitis (HSE), leading to a high mortality rate and severe neurological sequelae worldwide. HSE is typically accompanied by the blood-brain barrier (BBB) disruption, but the underlying mechanisms are unclear. To explore the disruption mechanisms of the BBB, quantitative analysis of the cellular proteome was carried out to investigate the proteomic changes that occur after infection. In this study, bEnd.3 cells were infected with HSV-1, followed by liquid chromatography-tandem mass spectrometry. A total of 6761 proteins were identified in three independent mass spectrometry analyses. Compared to the uninfected cells, 386 and 293 differentially expressed proteins were markedly upregulated or downregulated, respectively. Bioinformatic analysis showed that the activator protein-1 factor, including Fos, Jun, and ATF family proteins and cell adhesion molecules were significantly changed. Further validation of the changes observed for these proteins was carried out by western blotting and quantitative real-time PCR. Transendothelial electrical resistance (TEER) studies were performed to explore the effects of ATF3, Fra1, or JunB overexpression on the function of bEnd.3 cells. Characterization of the differential expression of these proteins in bEnd.3 cells will facilitate further exploration of BBB disruption upon HSV-1 infection.
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