ArticleThe Journal of clinical investigation1993
Replication of Marburg virus in human endothelial cells. A possible mechanism for the development of viral hemorrhagic disease.
Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 118 citations in OpenAlex.
- Potential Mechanisms Underlying Bleeding During Infection With Hemorrhagic Fever Viruses.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Emerging Strategies and Progress in the Medical Management of Marburg Virus Disease.Pathogens (Basel, Switzerland) · 2025Review
- Immunogenicity, Pathogenesis, and Host's Immuno-Responses to Marburg Virus Infection.Pathogens (Basel, Switzerland) · 2025Review
- Vascular dysfunction in hemorrhagic viral fevers: opportunities for organotypic modeling.Biofabrication · 2024Review
- Pathogenicity and virulence of Marburg virus.Virulence · 2022Review
- COVID-19-Associated Hyper-Fibrinolysis: Mechanism and Implementations.Frontiers in physiology · 2020Review
- Exchange Protein Directly Activated by cAMP Modulates Ebola Virus Uptake into Vascular Endothelial Cells.Viruses · 2018Article
- Marburg Virus Reverse Genetics Systems.Viruses · 2016Review
- Transcriptional Profiling of the Immune Response to Marburg Virus Infection.Journal of virology · 2015Article
- Mobilization of circulating endothelial progenitor cells correlates with the clinical course of hantavirus disease.Journal of virology · 2014Article
- Characterisation of a monoclonal antibody detecting Atlantic salmon endothelial and red blood cells, and its association with the infectious salmon anaemia virus cell receptor.Journal of anatomy · 2013Article
- Infectious salmon anaemia virus infection of Atlantic salmon gill epithelial cells.Virology journal · 2013Article
- Review
- Forty-five years of Marburg virus research.Viruses · 2012Review
- Expression of the infectious salmon anemia virus receptor on atlantic salmon endothelial cells correlates with the cell tropism of the virus.Journal of virology · 2012Article
- Human fatal zaire ebola virus infection is associated with an aberrant innate immunity and with massive lymphocyte apoptosis.PLoS neglected tropical diseases · 2010Article
- A filovirus-unique region of Ebola virus nucleoprotein confers aberrant migration and mediates its incorporation into virions.Journal of virology · 2008Article
- Immunopathogenesis of hantavirus pulmonary syndrome and hemorrhagic fever with renal syndrome: Do CD8+ T cells trigger capillary leakage in viral hemorrhagic fevers?Immunology letters · 2007Article
- Basolateral entry and release of Crimean-Congo hemorrhagic fever virus in polarized MDCK-1 cells.Journal of virology · 2007Article
- The temporal program of peripheral blood gene expression in the response of nonhuman primates to Ebola hemorrhagic fever.Genome biology · 2007Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Marburg and Ebola virus, members of the family Filoviridae, cause a severe hemorrhagic disease in humans and primates. The disease is characterized as a pantropic virus infection often resulting in a fulminating shock associated with hemorrhage, and death. All known histological and pathophysiological parameters of the disease are not sufficient to explain the devastating symptoms. Previous studies suggested a nonspecific destruction of the endothelium as a possible mechanism. Concerning the important regulatory functions of the endothelium (blood pressure, anti-thrombogenicity, homeostasis), we examined Marburg virus replication in primary cultures of human endothelial cells and organ cultures of human umbilical cord veins. We show here that Marburg virus replicates in endothelial cells almost as well as in monkey kidney cells commonly used for virus propagation. Our data support the concept that the destruction of endothelial cells resulting from Marburg virus replication is a possible mechanism responsible for the hemorrhagic disease and the shock syndrome typical of this infection.
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