ArticlePloS one2014
Hepatitis C virus induced endothelial inflammatory response depends on the functional expression of TNFα receptor subtype 2.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Thrombotic risk in hepatitis C: Interplay between hepatic dysfunction, viral-driven inflammation, and cardiovascular consequences.World journal of virology · 2025Review
- Chronic liver diseases and erectile dysfunction.Frontiers in public health · 2022Review
- Effects of Hepatitis C Virus Elimination by Direct-Acting Antiviral Agents on the Occurrence of Oral Lichen Planus and Periodontal Pathogen Load: A Preliminary Report.International journal of dentistry · 2021Article
- Article
- Extracellular Vesicle-Related Thrombosis in Viral Infection.International journal of general medicine · 2020Review
- Cardiovascular inflammation: RNA takes the lead.Journal of molecular and cellular cardiology · 2019Review
- Arterial thrombosis in the context of HCV-associated vascular disease can be prevented by protein C.Cellular & molecular immunology · 2017Article
- Macrophage Activation and the Tumor Necrosis Factor Cascade in Hepatitis C Disease Progression Among HIV-Infected Women Participating in the Women's Interagency HIV Study.Journal of acquired immune deficiency syndromes (1999) · 2017Article
- Double-stranded DNA induces a prothrombotic phenotype in the vascular endothelium.Scientific reports · 2017Article
- Mouse Hepatitis Virus Infection Induces a Toll-Like Receptor 2-Dependent Activation of Inflammatory Functions in Liver Sinusoidal Endothelial Cells during Acute Hepatitis.Journal of virology · 2016Article
- Is neutrophil gelatinase associated lipocalin useful in hepatitis C virus infection?World journal of hepatology · 2016Article
- Thrombin activation and liver inflammation in advanced hepatitis C virus infection.World journal of gastroenterology · 2016Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In hepatitis C virus (HCV) infection, morbidity and mortality often result from extrahepatic disease manifestations. We provide evidence for a role of receptors of the innate immune system in virally induced inflammation of the endothelium in vitro and in vivo. Corresponding to the in vitro finding of an HCV-dependent induction of proinflammatory mediators in endothelial cells, mice treated with poly (I:C) exhibit a significant reduction in leukocyte rolling velocity, an increase in leukocyte adhesion to the vessel wall and an increased extravasation of leukocytes. HCV directly promotes activation, adhesion and infiltration of inflammatory cells into the vessel wall by activation of endothelial viral receptors. Poly (I:C) induces the expression of TLR3 in vivo and hereby allows for amplification of all of the aforementioned responses upon viral infection. Proinflammatory effects of viral RNA are specifically mediated by TLR3 and significantly enhanced by tumor necrosis factor alpha (TNFα). HCV-RNA induces the endothelial expression of TNFα and TNFα receptor subtype 2 and we provide evidence that leucocyte adhesion and transmigration in response to activation of viral RNA receptors seem to depend on expression of functional TNFR2. Our results demonstrate that endothelial cells actively participate in immune mediated vascular inflammation caused by viral infections.
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