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Chromatin-Associated Regulation Of Hiv-1 Transcription

Implications for the development of therapeutic strategies

  • Chapter
Chromatin and Disease

Part of the book series: Subcellular Biochemistry ((SCBI,volume 41))

Human Immunodeficiency Virus type 1 (HIV-1) infection can now be treated effectively in many patients in the developed world, using combinations of antiretroviral therapeutics, called Highly Active Anti-Retroviral Therapy (HAART). However, despite prolonged treatment with HAART, the persistence of latently HIV-1-infected cellular reservoirs harboring transcriptionally silent but replication-competent proviruses represents the major hurdle to virus eradication. These latently infected cells are a permanent source for virus reactivation and lead to a rebound of the viral load after interruption of HAART. Therefore, a greater understanding of the molecular mechanisms regulating proviral latency and reactivation should lead to rational strategies aimed at purging these cellular reservoirs of HIV-1. This review summarizes our current knowledge and understanding of the elements involved in HIV-1 transcriptional reactivation: (1) the site of integration; (2) the transcription factor NF-κB, which is induced by proinflammatory cytokines (such as TNFα) and binds to two κB sites in the HIV-1 promoter region; (3) the specific remodeling of a single nucleosome (called nuc-1 and located immediately downstream of the HIV-1 transcription start site under latency conditions) upon activation of the HIV-1 promoter; (4) post-translational acetylation of histones and of non-histone proteins (following treatment with deacetylases inhibitors, which induce viral transcription and nuc-1 remodeling); and (5) the viral trans-activator Tat, which promotes transcription by mediating the recruitment to the HIV-1 promoter of histone-modifying enzymes and ATP-dependent chromatin remodeling complexes required for nucleosome disruption and transcriptional processivity. Finally, this review highlights experimental therapies aimed at administrating HIV-1 gene expression activators (such as HDAC inhibitors) combined with an effective HAART in order to reactivate and decrease/eliminate the pool of latently HIV-1-infected cellular reservoirs

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Authors and Affiliations

  1. Université Libre de Bruxelles (ULB), Institut de Biologie et de Médecine Moléculaires (IBMM), Laboratoire de Virologie Moléculaire, 12, rue des Professeurs Jeener et Brachet, 6041 Gosselies, Belgium

    Vincent Quivy, Stephane De Walque & Carine Van Lint

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  1. Vincent Quivy
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  2. Stephane De Walque
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  3. Carine Van Lint
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Editor information

Editors and Affiliations

  1. Jawaharlal Centre for Advanced Scientific Research, Jakkur, Bangalore, India

    Tapas K. Kundu

  2. Queens College,City University of New York, New York, USA

    R. Bittman

  3. Saha Institute of Nuclear Physics, Calcutta, India

    D. Dasgupta

  4. Max-Planck-Institute for Biochemistry, Munich, Germany

    H. Engelhardt

  5. MOLISA GmbH, Magdeburg, Germany

    L. Flohe

  6. German Cancer Research Center, Heidelberg, Germany

    H. Herrmann

  7. Texas A & M University, Texas, USA

    A. Holzenburg

  8. National University of Ireland, Galway, Ireland

    H-P. Nasheuer

  9. The Hebrew University, Jerusalem, Israel

    S. Rottem

  10. DSM Nutritional Products Ltd, Basel, Switzerland

    M. Wyss

  11. Max-Planck-Institute for Biochemistry, Munich, Germany

    P. Zwickl

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Quivy, V., Walque, S.D., Lint, C.V. (2007). Chromatin-Associated Regulation Of Hiv-1 Transcription. In: Kundu, T.K., et al. Chromatin and Disease. Subcellular Biochemistry, vol 41. Springer, Dordrecht. https://doi.org/10.1007/1-4020-5466-1_17

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