tailieunhanh - Báo cáo sinh học: " Actively replicating West Nile virus is resistant to cytoplasmic delivery of siRNA"

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: Actively replicating West Nile virus is resistant to cytoplasmic delivery of siRNA | Virology Journal BioMed Central Research Open Access Actively replicating West Nile virus is resistant to cytoplasmic delivery of siRNA Brian J Geiss1 Theodore C Pierson4 and Michael S Diamond 1 2 3 Address Departments of Medicine Washington University School of Medicine 660 South Euclid Avenue Box 8051 St. Louis MO 63110 USA 2Molecular Microbiology Washington University School of Medicine 660 South Euclid Avenue Box 8051 St. Louis MO 63110 USA 3Pathology Immunology Washington University School of Medicine 660 South Euclid Avenue Box 8051 St. Louis MO 63110 USA and 4Department of Microbiology University of Pennsylvania Philadelphia PA 19104 USA Email Brian J Geiss - Theodore C Pierson - piersontc@ Michael S Diamond - diamond@ Corresponding author Published 28 June 2005 Received 28 May 2005 Accepted 28 June 2005 Virology Journal 2005 2 53 doi 186 1743-422X-2-53 This article is available from http content 2 1 53 2005 Geiss 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 West Nile virus is an emerging human pathogen for which specific antiviral therapy has not been developed. Recent studies have suggested that RNA interference RNAi has therapeutic potential as a sequence specific inhibitor of viral infection. Here we examine the ability of exogenous small interfering RNAs siRNAs to block the replication of West Nile virus in human cells. Results WNV replication and infection was greatly reduced when siRNA were introduced by cytoplasmic-targeted transfection prior to but not after the establishment of viral replication. WNV appeared to evade rather than actively block the RNAi machinery as sequence-specific reduction in .