Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Molecular basis of telaprevir resistance due to V36 and T54 mutations in the NS3-4A protease of the hepatitis C virus. | Open Access Molecular basis of telaprevir resistance due to V36 and T54 mutations in the NS3-4A protease of the hepatitis C virus Christoph WelschH n Francisco S Domingues Simone Sussern Iris Antes Christoph Hartmann Gabriele Mayr Andreas Schlicker Christoph Sarrazin Mario Albrecht Stefan Zeuzemn and Thomas Lengauer Addresses Department of Computational Biology and Applied Algorithmics Max Planck Institute for Informatics 66123 Saarbrucken Germany. Department of Internal Medicine I Johann Wolfgang Goethe University Hospital 60590 Frankfurt Main Germany. Department of Internal Medicine II Saarland University Hospital 66421 Homburg Saar Germany. H These authors contributed equally to this work. Correspondence Christoph Welsch. Email christophwelsch@ Published 23 January 2008 Genome Biology 2008 9 R16 doi gb-2008-9-l-rl6 The electronic version of this article is the complete one and can be found online at http 2008 9 l Rl6 Received 17 July 2007 Revised 17 November 2007 Accepted 23 January 2008 2008 Welsch 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 Background The inhibitor telaprevir VX-950 of the hepatitis C virus HCV protease NS3-4A has been tested in a recent phase lb clinical trial in patients infected with HCV genotype l. This trial revealed residue mutations that confer varying degrees of drug resistance. In particular two protease positions with the mutations V36A G L M and T54A S were associated with low to medium levels of drug resistance during viral breakthrough together with only an intermediate reduction of viral replication fitness. These mutations are located in the protein interior and far away from the ligand binding pocket. Results Based on the available .
