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Conference highlights of the 5th international workshop on HIV persistence during therapy, 6-9 December 2011, St. Maartin, West Indies

DOI: 10.1186/1742-6405-9-7

Keywords: HIV persistence, HIV reservoirs, HIV latency, HIV cure, HIV eradication, HIV reservoir group

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Abstract:

The 5th international workshop on HIV persistence during therapy was held in St. Maarten from December 6-9 and featured presentations from 210 scientists representing approximately 10 countries. Since its inception, the goal of the workshop has been to provide a forum for research aimed at understanding the mechanism by which HIV-1 persists in the face of antiretroviral therapy (ART) and to develop strategies with which to curtail viral persistence and accelerate the objective of viral eradication. While ART has fundamentally impacted the health of individuals living with HIV infection and effects durable suppression of plasma viral RNA to undetectable levels, current treatment regimens are unable to eradicate the virus [1]. In addition, pathogenic manifestations of HIV-1 infection are manifest despite potent viral suppression. Therefore, it is clear that we have to look beyond long-term maintenance of HIV-1 infection and ultimately develop strategies for viral eradication.The development of strategies to eliminate HIV-1 reservoirs that persist in the face of ART will require a complete understanding of the nature of viral persistence and latency and how these processes are regulated. While latency is considered the single biggest obstacle to viral eradication, how latency is established and regulated is still not well understood. Most of the studies conducted to date on viral latency have focused on models that employ established cell lines. They have demonstrated various forms of latency regulation and the role of host cell cycle, epigenetic effects and other host cell factors that can regulate viral latency. However, it is unclear as to the extent to which these cell line models of viral latency reflect the true nature of latency as it exists in memory CD4+ T cells [2]. For this reason, several investigators have attempted to develop primary cell models of viral latency so as to gain greater physiologic insight into viral persistence and latency and more importan

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