ArticleGut2016
Modulation of HCV reinfection after orthotopic liver transplantation by fibroblast growth factor-2 and other non-interferon mediators.
Article in Gut, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- IFNL4-rs12979860 CC genotype predisposes to accelerated terminal exhaustion and senescence in HIV/HCV-chronic infection.Journal of translational medicine · 2025Article
- FGF receptor kinase inhibitors exhibit broad antiviral activity by targeting Src family kinases.Cellular and molecular life sciences : CMLS · 2024Article
- Cytokine profile and viral diversity in the early seronegative stage of community-acquired hepatitis C virus (HCV) infection.Scientific reports · 2023Article
- Antagonism of interferon signaling by fibroblast growth factors promotes viral replication.EMBO molecular medicine · 2020Article
- Fibroblast Growth Factor 2 Enhances Zika Virus Infection in Human Fetal Brain.The Journal of infectious diseases · 2019Article
- Wnt/β-Catenin Signaling in Liver Cancers.Cancers · 2019Review
- Action and function of Wnt/β-catenin signaling in the progression from chronic hepatitis C to hepatocellular carcinoma.Journal of gastroenterology · 2017Review
- High resolution sequencing of hepatitis C virus reveals limited intra-hepatic compartmentalization in end-stage liver disease.Journal of hepatology · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIn HCV infected individuals graft infection occurs shortly after orthotopic liver transplantation (OLT). We aimed to describe the composition of the inflammatory response at this time, how it affects the HCV replication cycle and identify novel proviral and antiviral factors.
designWe used a Luminex assay to quantify 50 inflammatory mediators in sera before and shortly after OLT. In vitro grown HCV based on the JFH-1 isolate were used to characterise the effects of patient sera and individual mediators on HCV.
resultsAlthough the mediator composition is highly variable between individuals, sera drawn immediately post-OLT significantly enhance HCV infectivity compared with control sera from before OLT in about half of the cases. Among 27 non-interferon inflammatory mediators fibroblast growth factor (FGF)-2 stood out as it enhanced HCV RNA replication and release of infectious particles. The effect was concentration-dependent and detectable in dividing and non-dividing cells. Moreover, pharmacological inhibition of FGF-2 receptor signalling abrogated the enhancing effect of FGF-2 and inhibited HCV replication in the absence of serum FGF-2 suggesting that HCV replication is dependent on basal activation of the FGF-2 triggered signalling pathway. Finally, in individuals with chronic HCV infection with high viral load, serum FGF-2 was significantly higher compared with those with low viral load.
conclusionsAlthough no single mediator may account for this effect, serum shortly post-OLT enhances HCV infection. FGF-2 is a novel endogenous driver of HCV replication and a potential therapeutic target.
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