Tuyển tập các báo cáo nghiên cứu về hóa học được đăng trên tạp chí sinh học đề tài :Effect of ethanol on innate antiviral pathways and HCV replication in human liver cells | Virology Journal BioMed Central Research Open Access Effect of ethanol on innate antiviral pathways and HCV replication in human liver cells Courtney R Plumlee1 2 Catherine A Lazaro3 Nelson Fausto4 and Stephen J Polyak 5 Address Department of Laboratory Medicine University of Washington Seattle USA 2Department of Biological Sciences Columbia University New York NY 3Department of Pathology University of Washington Seattle USA 4Department of Pathology University of Washington Seattle USA and 5Departments of Laboratory Medicine Microbiology and Pathobiology University of Washington Seattle USA Email Courtney R Plumlee - crp2109@ Catherine A Lazaro - clazaro@ Nelson Fausto - nfausto@ Stephen J Polyak - polyak@ Corresponding author Published 02 December 2005 Received 06 September 2005 Accepted 02 December 2005 Virology Journal 2005 2 89 doi 1743-422X-2-89 This article is available from http content 2 1 89 2005 Plumlee et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Alcohol abuse reduces response rates to IFN therapy in patients with chronic hepatitis C. To model the molecular mechanisms behind this phenotype we characterized the effects of ethanol on Jak-Stat and MAPK pathways in Huh7 human hepatoma cells in HCV replicon cell lines and in primary human hepatocytes. High physiological concentrations of acute ethanol activated the Jak-Stat and p38 MAPK pathways and inhibited HCV replication in several independent replicon cell lines. Moreover acute ethanol induced Statl serine phosphorylation which was partially mediated by the p38 MAPK pathway. In contrast when combined with exogenously applied IFN-a ethanol inhibited the .
