ArticleJournal of virology2008
Measles virus-induced block of transendothelial migration of T lymphocytes and infection-mediated virus spread across endothelial cell barriers.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- Hepatitis E virus infects brain microvascular endothelial cells, crosses the blood-brain barrier, and invades the central nervous system.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Role of Dendritic Cells in Viral Brain Infections.Frontiers in immunology · 2022Review
- Article
- Neurocognitive impacts of arbovirus infections.Journal of neuroinflammation · 2020Review
- Enterovirus A71 capsid protein VP1 increases blood-brain barrier permeability and virus receptor vimentin on the brain endothelial cells.Journal of neurovirology · 2020Article
- A Co-culture Method to Investigate the Crosstalk Between X-ray Irradiated Caco-2 Cells and PBMC.Journal of visualized experiments : JoVE · 2018Article
- Microorganisms' Footprint in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2018Review
- Nipah Virus Infection of Immature Dendritic Cells Increases Its Transendothelial Migration Across Human Brain Microvascular Endothelial Cells.Frontiers in microbiology · 2018Article
- Article
- Immune Regulation of Antibody Access to Neuronal Tissues.Trends in molecular medicine · 2017Review
- Keeping it in check: chronic viral infection and antiviral immunity in the brain.Nature reviews. Neuroscience · 2016Review
- Measles Virus Host Invasion and Pathogenesis.Viruses · 2016Review
- Mechanisms of restriction of viral neuroinvasion at the blood-brain barrier.Current opinion in immunology · 2016Review
- Measles virus, immune control, and persistence.FEMS microbiology reviews · 2012Review
- Review
- Nipah virus infection and glycoprotein targeting in endothelial cells.Virology journal · 2010Article
- Measles virus infection of the CNS: human disease, animal models, and approaches to therapy.Medical microbiology and immunology · 2010Review
- Measles virus-induced suppression of immune responses.Immunological reviews · 2010Review
- Porcine circovirus 2 (PCV2) increases the expression of endothelial adhesion/junction molecules.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In order to analyze whether measles virus (MV) is transported via transmigrating leukocytes across endothelial barriers or whether virus spreads via infection of endothelial cells and basolateral release, we investigated the migratory behavior of infected human primary T lymphocytes across polarized cell layers of human brain microvascular endothelial cells. We found that the capacity of lymphocytes to migrate through filter pores was only slightly affected by wild-type MV infection, whereas their capacity to migrate through endothelial barriers was drastically reduced. MV infection stimulated the expression and activation of the leukocyte integrins LFA-1 and VLA-4, mediating a strong adherence to the surface of endothelial cells. Furthermore, the formation of engulfing membrane protrusions by endothelial cells, so-called transmigratory cups, was induced, but transmigration was impaired. As a consequence of this close cell-cell contact, MV infection was transmitted from lymphocytes to the endothelium. MV envelope proteins were expressed on the apical and basolateral surfaces of infected polarized endothelial cells, and virus was released from both sides. Wild-type MV infection did not induce the formation of syncytia, suggesting virus spread from cell to cell via cell processes and contacts. Our data indicate that transendothelial migration of infected T cells is strongly inhibited, whereas virus can cross endothelial barriers by productive infection of the endothelium and subsequent bipolar virus release.
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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.