ArticleNature chemical biology2016
Nuclear receptors control pro-viral and antiviral metabolic responses to hepatitis C virus infection.
Article in Nature chemical biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 52 citations in OpenAlex.
- Trial
- HBV/HCV coinfection and anti-tuberculosis drug-induced liver injury: from risk assessment and exploration of mechanisms to preventive considerations.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Review
- Bovine viral diarrhea virus (BVDV) relies on cellular lipid droplet biogenesis and lipolysis to provide energy for viral replication.Veterinary research · 2026Article
- Pestivirus bovine viral diarrhea virus infection induces ROS-HIF-1a axis-driven glycolytic reprogramming, which increases viral replication by impairing RIG-I-dependent type I interferon response.Journal of virology · 2026Article
- Nuclear receptors in health and disease: signaling pathways, biological functions and pharmaceutical interventions.Signal transduction and targeted therapy · 2025Review
- Association between metabolic associated fatty liver disease and HCC risk after SVR in HCV patients: A systematic review and meta-analysis.Clinical and experimental hepatology · 2025Article
- Article
- Farnesoid X receptor: From Structure to Function and Its Pharmacology in Liver Fibrosis.Aging and disease · 2024Review
- Metabolic Reprogramming of HCC: A New Microenvironment for Immune Responses.International journal of molecular sciences · 2023Review
- NRF2 activation induces NADH-reductive stress, providing a metabolic vulnerability in lung cancer.Cell metabolism · 2023Article
- Transcriptional Inhibition of MicroRNA miR-122 by Small Molecules Reduces Hepatitis C Virus Replication in Liver Cells.Journal of medicinal chemistry · 2022Article
- microRNA-27b regulates hepatic lipase enzyme LIPC and reduces triglyceride degradation during hepatitis C virus infection.The Journal of biological chemistry · 2022Article
- What role for cellular metabolism in the control of hepatitis viruses?Frontiers in immunology · 2022Review
- A Review of Emerging Goose Astrovirus Causing Gout.BioMed research international · 2022Review
- Review
- Initial HCV infection of adult hepatocytes triggers a temporally structured transcriptional program containing diverse pro- and anti-viral elements.Journal of virology · 2021Article
- Mechanism and reversal of drug-induced nephrotoxicity on a chip.Science translational medicine · 2021Article
- SPARC Overexpression Promotes Liver Cancer Cell Proliferation and Tumor Growth.Frontiers in molecular biosciences · 2021Article
- Metabolic alterations and vulnerabilities in hepatocellular carcinoma.Gastroenterology report · 2021Review
- Liver-expressedScience advances · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 7 institutions in 4 countries.
Funding
Abstract
Viruses lack the basic machinery needed to replicate and therefore must hijack the host's metabolism to propagate. Virus-induced metabolic changes have yet to be systematically studied in the context of host transcriptional regulation, and such studies shoul offer insight into host-pathogen metabolic interplay. In this work we identified hepatitis C virus (HCV)-responsive regulators by coupling system-wide metabolic-flux analysis with targeted perturbation of nuclear receptors in primary human hepatocytes. We found HCV-induced upregulation of glycolysis, ketogenesis and drug metabolism, with glycolysis controlled by activation of HNF4α, ketogenesis by PPARα and FXR, and drug metabolism by PXR. Pharmaceutical inhibition of HNF4α reversed HCV-induced glycolysis, blocking viral replication while increasing apoptosis in infected cells showing virus-induced dependence on glycolysis. In contrast, pharmaceutical inhibition of PPARα or FXR reversed HCV-induced ketogenesis but increased viral replication, demonstrating a novel host antiviral response. Our results show that virus-induced changes to a host's metabolism can be detrimental to its life cycle, thus revealing a biologically complex relationship between virus and host.
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What OpenQuestion holds
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.