Retrovirology Research BioMed Central Open Access HIV-1 latency in actively dividing human T cell

Retrovirology Research BioMed Central Open Access HIV-1 latency in actively dividing human T cell lines Rienk E Jeeninga, Ellen M Westerhout, Marja L van Gerven and Ben Berkhout* Address: Laboratory of Experimental Virology, Department of Medical Microbiology, Center for Infection and Immunity Amsterdam (CINIMA), Academic Medical Center, University of Amsterdam, The Netherlands Email: Rienk E Jeeninga - ; Ellen M Westerhout - ; Marja L van Gerven - ; Ben Berkhout* - * Corresponding author Published: 25 April 2008 Retrovirology 2008, 5:37 doi: Received: 19 March 2008 Accepted: 25 April 2008 This article is available from: © 2008 Jeeninga et al; licensee BioMed Central Ltd. This is. | Retrovirology BioMed Central Research HIV-1 latency in actively dividing human T cell lines Rienk E Jeeninga Ellen M Westerhout Marja L van Gerven and Ben Berkhout Open Access Address Laboratory of Experimental Virology Department of Medical Microbiology Center for Infection and Immunity Amsterdam CINIMA Academic Medical Center University of Amsterdam The Netherlands Email Rienk E Jeeninga - Ellen M Westerhout - Marja L van Gerven - Ben Berkhout - Corresponding author Published 25 April 2008 Received 19 March 2008 Retrovirology 2008 5 37 doi 1742-4690-5-37 Accepted 25 April 2008 This article is available from http content 5 1 37 2008 Jeeninga 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 Eradication of HIV-1 from an infected individual cannot be achieved by current drug regimens. Viral reservoirs established early during the infection remain unaffected by anti-retroviral therapy and are able to replenish systemic infection upon interruption of the treatment. Therapeutic targeting of viral latency will require a better understanding of the basic mechanisms underlying the establishment and long-term maintenance of HIV-1 in resting memory CD4 T cells the most prominent reservoir of transcriptional silent provirus. However the molecular mechanisms that permit long-term transcriptional control of proviral gene expression in these cells are still not well understood. Exploring the molecular details of viral latency will provide new insights for eventual future therapeutics that aim at viral eradication. Results We set out to develop a new in vitro HIV-1 latency model system using

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