tailieunhanh - Báo cáo y học: "Akt inhibitors as an HIV-1 infected macrophage-specific anti-viral therapy"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: "Akt inhibitors as an HIV-1 infected macrophage-specific anti-viral therapy. | Retrovirology BioMed Central Research Akt inhibitors as an HIV-1 infected macrophage-specific anti-viral therapy Pauline Chugh 1 Birgit Bradel-Tretheway1 Carlos MR Monteiro-Filho2 Vicente Planelles2 Sanjay B Maggirwar1 Stephen Dewhurst1 and Baek Kim 1 Open Access Address Department of Microbiology and Immunology School of Medicine University of Rochester Medical Center 601 Elmwood Avenue Box 672 Rochester New York 14742 USA and 2Division of Cellular Biology and Immunology Department of Pathology University of Utah School of Medicine 30 N 1900 East SOM 5C210 Salt Lake City UT 84132. USA Email Pauline Chugh - Pauline_Chugh@ Birgit Bradel-Tretheway - Birgit_bradeltretheway@ Carlos MR Monteiro-Filho - Baek_Kim@ Vicente Planelles - Baek_Kim@ Sanjay B Maggirwar - Sanjay_Maggirwar@ Stephen Dewhurst - Stephen_Dewhurst@ Baek Kim - Baek_Kim@ Corresponding author Published 31 January 2008 Received 12 December 2007 Accepted 31 January 2008 Retrovirology 2008 5 11 doi l 742-4690-5-1 I This article is available from http content 5 1 1 1 2008 Chugh 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 Unlike CD4 T cells HIV-1 infected macrophages exhibit extended life span even upon stress consistent with their in vivo role as long-lived HIV-1 reservoirs. Results Here we demonstrate that PI3K Akt inhibitors including clinically available Miltefosine dramatically reduced HIV-1 production from long-living virus-infected macrophages. These PI3K Akt inhibitors hyper-sensitize infected macrophages to extracellular stresses that they are normally exposed to and eventually