tailieunhanh - Báo cáo hóa học: " Arbidol: a broad-spectrum antiviral that inhibits acute and chronic HCV infection"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Arbidol: a broad-spectrum antiviral that inhibits acute and chronic HCV infection | Virology Journal BioMed Central Research Arbidol a broad-spectrum antiviral that inhibits acute and chronic HCV infection Yury S Boriskin1 3 Eve-Isabelle Pécheur2 and Stephen J Polyak 1 Open Access Address Departments of Laboratory Medicine Microbiology and Pathobiology University of Washington Seattle USA 2IFR128 Biosciences Lyon Gerland Institut de Biologie et Chimie des Protéines UMR 5086 CNRS-Université Claude Bernard Lyon I Lyon France and Institute of Virology Moscow Russia Email Yury S Boriskin - yboriskin@ Eve-Isabelle Pécheur - Stephen J Polyak - polyak@ Corresponding author Published 19 July 2006 Received 02 June 2006 Accepted 19 July 2006 Virology journal 2006 3 56 doi 186 1743-422X-3-56 This article is available from http content 3 1 56 2006 Boriskin 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 Arbidol ARB is an antiviral compound that was originally proven effective for treatment of influenza and several other respiratory viral infections. The broad spectrum of ARB anti-viral activity led us to evaluate its effect on hepatitis C virus HCV infection and replication in cell culture. Long-term ARB treatment of Huh7 cells chronically replicating a genomic length genotype 1b replicon resulted in sustained reduction of viral RNA and protein expression and eventually cured HCV infected cells. Pre-treatment of human hepatoma cells with 15 pM ARB for 24 to 48 hours inhibited acute infection with JFH-1 virus by up to 1000-fold. The inhibitory effect of ARB on HCV was not due to generalized cytotoxicity nor to augmentation of IFN antiviral signaling pathways but involved impaired virus-mediated membrane fusion. ARB s affinity for