Interferon-stimulated genes and their role in controlling hepatitis C virus
| Autor: | Ralf Bartenschlager, Philippe Metz, Silke Bender, Antje Reuter |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Oxidoreductases Acting on CH-CH Group Donors
Hepatitis C virus Hepacivirus Biology Virus Replication medicine.disease_cause Chronic liver disease Virus DEAD-box RNA Helicases eIF-2 Kinase Liver disease Interferon 2' 5'-Oligoadenylate Synthetase medicine Humans Receptors Immunologic Mode of action Interferon-stimulated genes Gene Hepatology Toll-Like Receptors Proteins virus diseases medicine.disease Antigens Differentiation Virology Viral replication Immunology DEAD Box Protein 58 Interferons medicine.drug |
| Zdroj: | ResearcherID |
| ISSN: | 0168-8278 |
| DOI: | 10.1016/j.jhep.2013.07.033 |
| Popis: | SummaryInfections with the hepatitis C virus (HCV) are a major cause of chronic liver disease. While the acute phase of infection is mostly asymptomatic, this virus has the high propensity to establish persistence and in the course of one to several decades liver disease can develop. HCV is a paradigm for the complex interplay between the interferon (IFN) system and viral countermeasures. The virus induces an IFN response within the infected cell and is rather sensitive against the antiviral state triggered by IFNs, yet in most cases HCV persists. Numerous IFN-stimulated genes (ISGs) have been reported to suppress HCV replication, but in only a few cases we begin to understand the molecular mechanisms underlying antiviral activity. It is becoming increasingly clear that blockage of viral replication is mediated by the concerted action of multiple ISGs that target different steps of the HCV replication cycle. This review briefly summarizes the activation of the IFN system by HCV and then focuses on ISGs targeting the HCV replication cycle and their possible mode of action. |
| Databáze: | OpenAIRE |
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