title: [The role of hepcidin and polymorphisms in the regulatory region of the IL-28B gene in HCV infections].
abstract: HCV infection is a big problem worldwide. The virus is the main cause of chronic hepatitis and liver cirrhosis. The common treatment is based on a combination of pegylated IFN‑α and ribavirin. It leads to SVR in 40-52% of HCV-1-infected patients and more than 70% of HCV-2- or HCV-3-infected individuals. Unfortunately, this therapy is only partially effective, expensive and associated with numerous side effects. To improve the response, especially among individuals infected with genotype 1, which is the most resistant to standard therapy, new strategies are sought. In 2011 the US FDA licensed two agents, boceprevir and telaprevir, which are protease inhibitors. In the future triple therapy (pegIFN-α/RBV/protease inhibitor) may be the standard of care for patients infected with HCV-1. Polymorphisms in the regulatory region of the Il-28B gene (SNP rs12979860, SNP rs8099917) play a very important role in predicting treatment outcome. They are also associated with spontaneous recovery from HCV infection and explain the difference in response to standard therapy between the black and white races. Personalized therapy, which is defined as suitable treatment for the right patient, should become the main treatment strategy for HCV-infected individuals. It could be possible to make the therapy more effective and safe. Hepcidin is a hormone regulating iron metabolism. A low level of hepcidin leads to iron overload then to inflammation and liver fibrosis. It is observed in HCV-infected patients. Iron influence over HCV replication is not distinctly determined.
authors.affiliation: Zakład Biochemii Medycznej Uniwersytetu Medycznego w Łodzi.
authors.forename: Magdalena
authors.initials: M
authors.lastname: Cybula
authors.affiliation: Zakład Biochemii Medycznej Uniwersytetu Medycznego w Łodzi.
authors.forename: Janusz
authors.initials: J
authors.lastname: Szemraj
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000008:administration & dosage; D004359:Drug Therapy, Combination; D016174:Hepacivirus / Q000187:drug effects; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000235:genetics* / Q000378:metabolism; D064451:Hepcidins / Q000378:metabolism*; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use; D007372:Interferons; D007378:Interleukins / Q000235:genetics*; D009842:Oligopeptides / Q000008:administration & dosage; D011110:Polymorphism, Genetic; D011379:Prognosis; D011392:Proline / Q000008:administration & dosage / Q000031:analogs & derivatives; D011480:Protease Inhibitors / Q000008:administration & dosage; D012045:Regulatory Sequences, Nucleic Acid; D012254:Ribavirin / Q000627:therapeutic use; D016896:Treatment Outcome; D000095022:Interferon Lambda
chemical_list: D000998:Antiviral Agents; D064451:Hepcidins; D016898:Interferon-alpha; D007372:Interferons; D007378:Interleukins; D009842:Oligopeptides; D011392:Proline; D011480:Protease Inhibitors; D012254:Ribavirin; C000624353:interferon-lambda, human; D000095022:Interferon Lambda; C486464:telaprevir; C512204:N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide