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Báo cáo y học: "Molecular control of HIV-1 postintegration latency: implications for the development of new therapeutic strategies"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Retrovirology cung cấp cho các bạn kiến thức về ngành y đề tài: Molecular control of HIV-1 postintegration latency: implications for the development of new therapeutic strategies. | Retrovirology BioMed Central Open Access Review Molecular control of HIV-1 postintegration latency implications for the development of new therapeutic strategies Laurence Colin and Carine Van Lint Address Laboratory of Molecular Virology Institut de Biologie et de Médecine Moléculaires IBMM Université Libre de Bruxelles ULB 6041 Gosselies Belgium Email Laurence Colin - lcolin@ulb.ac.be Carine Van Lint - cvlint@ulb.ac.be Corresponding author Published 4 December 2009 Received I November 2009 Accepted 4 December 2009 Retrovirology 2009 6 111 doi 10.1186 1742-4690-6-111 This article is available from http www.retrovirology.com content 6 I III 2009 Colin and Van Lint licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract The persistence of HIV-1 latent reservoirs represents a major barrier to virus eradication in infected patients under HAART since interruption of the treatment inevitably leads to a rebound of plasma viremia. Latency establishes early after infection notably but not only in resting memory CD4 T cells and involves numerous host and viral trans-acting proteins as well as processes such as transcriptional interference RNA silencing epigenetic modifications and chromatin organization. In order to eliminate latent reservoirs new strategies are envisaged and consist of reactivating HIV-1 transcription in latently-infected cells while maintaining HAART in order to prevent de novo infection. The difficulty lies in the fact that a single residual latently-infected cell can in theory rekindle the infection. Here we review our current understanding of the molecular mechanisms involved in the establishment and maintenance of HIV-1 latency and in the transcriptional reactivation from latency. We highlight the potential of