scholarly journals Transcriptome Signature of Nipah Virus Infected Endothelial Cells

10.5772/21512 ◽  
2011 ◽  
Author(s):  
Mathieu Cyrille ◽  
Legras-Lachuer Catherine ◽  
Horvat Brank
Keyword(s):  
Endothelial Cells ◽  
Nipah Virus ◽  
Transcriptome Signature

scholarly journals Differential Innate Immune Responses Elicited by Nipah Virus and Cedar Virus Correlate with Disparate In Vivo Pathogenesis in Hamsters

Viruses ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 291 ◽  
Author(s):  
Tony Schountz ◽  
Corey Campbell ◽  
Kaitlyn Wagner ◽  
Joel Rovnak ◽  
Cynthia Martellaro ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Syrian Hamster ◽  
Nipah Virus ◽  
Neutralizing Antibody ◽  
Type I ◽  
Type I Ifn ◽  
Innate Immune Responses ◽  
Syrian Hamsters ◽  
Pulmonary Endothelial Cells

Syrian hamsters (Mesocricetus auratus) are a pathogenesis model for the Nipah virus (NiV), and we sought to determine if they are also susceptible to the Cedar virus (CedPV). Following intranasal inoculation with CedPV, virus replication occurred in the lungs and spleens of infected hamsters, a neutralizing antibody was produced in some hamsters within 8 days post-challenge, and no conspicuous signs of disease occurred. CedPV replicated to a similar magnitude as NiV-Bangladesh in type I IFN-deficient BHK-21 Syrian hamster fibroblasts but replicated 4 logs lower in type I IFN-competent primary Syrian hamster and human pulmonary endothelial cells, a principal target of henipaviruses. The coinfection of these cells with CedPV and NiV failed to rescue CedPV titers and did not diminish NiV titers, suggesting the replication machinery is virus-specific. Type I IFN response transcripts Ifna7, Ddx58, Stat1, Stat2, Ccl5, Cxcl10, Isg20, Irf7, and Iigp1 were all significantly elevated in CedPV-infected hamster endothelial cells, whereas Ifna7 and Iigp1 expression were significantly repressed during NiV infection. These results are consistent with the hypothesis that CedPV’s inability to counter the host type I IFN response may, in part, contribute to its lack of pathogenicity. Because NiV causes a fatal disease in Syrian hamsters with similarities to human disease, this model will provide valuable information about the pathogenic mechanisms of henipaviruses.

scholarly journals Selective receptor expression restricts Nipah virus infection of endothelial cells

2008 ◽  
Vol 5 (1) ◽  
pp. 142 ◽  
Author(s):  
Stephanie Erbar ◽  
Sandra Diederich ◽  
Andrea Maisner
Keyword(s):  
Endothelial Cells ◽  
Virus Infection ◽  
Nipah Virus ◽  
Receptor Expression

scholarly journals Timing of Galectin-1 Exposure Differentially Modulates Nipah Virus Entry and Syncytium Formation in Endothelial Cells

2014 ◽  
Vol 89 (5) ◽  
pp. 2520-2529 ◽  
Author(s):  
Omai B. Garner ◽  
Tatyana Yun ◽  
Olivier Pernet ◽  
Hector C. Aguilar ◽  
Arnold Park ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Virus Infection ◽  
Host Cell ◽  
Cell Fusion ◽  
Nipah Virus ◽  
Syncytium Formation ◽  
Progeny Virus ◽  
Human Endothelial Cells ◽  
Opposing Effects

ABSTRACTNipah virus (NiV) is a deadly emerging enveloped paramyxovirus that primarily targets human endothelial cells. Endothelial cells express the innate immune effector galectin-1 that we have previously shown can bind to specific N-glycans on the NiV envelope fusion glycoprotein (F). NiV-F mediates fusion of infected endothelial cells into syncytia, resulting in endothelial disruption and hemorrhage. Galectin-1 is an endogenous carbohydrate-binding protein that binds to specific glycans on NiV-F to reduce endothelial cell fusion, an effect that may reduce pathophysiologic sequelae of NiV infection. However, galectins play multiple roles in regulating host-pathogen interactions; for example, galectins can promote attachment of HIV to T cells and macrophages and attachment of HSV-1 to keratinocytes but can also inhibit influenza entry into airway epithelial cells. Using live Nipah virus, in the present study, we demonstrate that galectin-1 can enhance NiV attachment to and infection of primary human endothelial cells by bridging glycans on the viral envelope to host cell glycoproteins. In order to exhibit an enhancing effect, galectin-1 must be present during the initial phase of virus attachment; in contrast, addition of galectin-1 postinfection results in reduced production of progeny virus and syncytium formation. Thus, galectin-1 can have dual and opposing effects on NiV infection of human endothelial cells. While various roles for galectin family members in microbial-host interactions have been described, we report opposing effects of the same galectin family member on a specific virus, with the timing of exposure during the viral life cycle determining the outcome.IMPORTANCENipah virus is an emerging pathogen that targets endothelial cells lining blood vessels; the high mortality rate (up to 70%) in Nipah virus infections results from destruction of these cells and resulting catastrophic hemorrhage. Host factors that promote or prevent Nipah virus infection are not well understood. Endogenous human lectins, such as galectin-1, can function as pattern recognition receptors to reduce infection and initiate immune responses; however, lectins can also be exploited by microbes to enhance infection of host cells. We found that galectin-1, which is made by inflamed endothelial cells, can both promote Nipah virus infection of endothelial cells by “bridging” the virus to the cell, as well as reduce production of progeny virus and reduce endothelial cell fusion and damage, depending on timing of galectin-1 exposure. This is the first report of spatiotemporal opposing effects of a host lectin for a virus in one type of host cell.

scholarly journals Characterization of the antiviral and inflammatory responses against Nipah virus in endothelial cells and neurons

Virology ◽  
2010 ◽  
Vol 404 (1) ◽  
pp. 78-88 ◽  
Author(s):  
Michael K. Lo ◽  
David Miller ◽  
Mohammad Aljofan ◽  
Bruce A. Mungall ◽  
Pierre E. Rollin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Responses ◽  
Nipah Virus

scholarly journals Early Activation of Primary Brain Microvascular Endothelial Cells by Nipah Virus Glycoprotein-Containing Particles

2015 ◽  
Vol 90 (5) ◽  
pp. 2706-2709 ◽  
Author(s):  
Tanja C. Freitag ◽  
Andrea Maisner
Keyword(s):  
Central Nervous System ◽  
Endothelial Cells ◽  
Nervous System ◽  
Nipah Virus ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Cns Inflammation ◽  
Highly Pathogenic ◽  
Cytokine Induction ◽  
Microvascular Endothelial

Nipah virus (NiV) is a highly pathogenic paramyxovirus that causes pronounced infection of brain endothelia and central nervous system (CNS) inflammation. Using primary porcine brain microvascular endothelial cells, we showed that upregulation of E-selectin precedes cytokine induction and is induced not only by infectious NiV but also by NiV-glycoprotein-containing virus-like particles. This demonstrates that very early events in NiV brain endothelial infection do not depend on NiV replication but can be triggered by the NiV glycoproteins alone.

Endotoxin Alteration of the Mucopolysaccharide Blood Vessel Coating in Rats

1974 ◽  
Vol 32 ◽  
pp. 148-149
Author(s):  
D. E. Philpott ◽  
A. Takahashi
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Salivary Gland ◽  
Carotid Artery ◽  
Basement Membrane ◽  
Coronary Vessels ◽  
Ruthenium Red ◽  
E Coli ◽  
Old Rats ◽  
The Brain

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.

Complex Vesicles, Microtubules, and Cytoplasmic Filaments in the Endothelial Cells of Normal Dog Aorta

1968 ◽  
Vol 26 ◽  
pp. 172-173
Author(s):  
C. N. Sun ◽  
J. J. Ghidoni
Keyword(s):  
Electron Microscopy ◽  
Endothelial Cells ◽  
Cross Sections ◽  
Functional Significance ◽  
Tubular Structures ◽  
Aldehyde Fixation ◽  
Cytoplasmic Filaments

Endothelial cells in longitudinal and cross sections of aortas from 3 randomly selected “normal” mongrel dogs were studied by electron microscopy. Segments of aorta were distended with cold cacodylate buffered 5% glutaraldehyde for 10 minutes prior to being cut into small, well oriented tissue blocks. After an additional 1-1/2 hour period in glutaraldehyde, the tissue blocks were well rinsed in buffer and post-fixed in OsO4. After dehydration they were embedded in a mixture of Maraglas, D.E.R. 732, and DDSA.Aldehyde fixation preserves the filamentous and tubular structures (300 Å and less) for adequate demonstration and study. The functional significance of filaments and microtubules has been recently discussed by Buckley and Porter; the precise roles of these cytoplasmic components remains problematic. Endothelial cells in canine aortas contained an abundance of both types of structures.

Sign in / Sign up

Export Citation Format

Share Document