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Chromatin Control of HIV-1 Gene Expression

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Structural Biology and Functional Genomics

Part of the book series: NATO Science Series ((ASHT,volume 71))

Abstract

Upon infection of susceptible cells, the RNA genome of the human immunodeficiency virus type 1 (HIV-1) is reverse transcribed into double-stranded DNA, which can be subsequently integrated into the cellular genome. After integration, the viral long terminal repeat (LTR) promoter is present in a nucleosome-bound conformation and is transcriptionally silent in the absence of stimulation. Activation of HIV-I gene expression is concomitant with an acetylation-dependent rearrangement of the nucleosome positioned at the viral transcription start site. Thus, similar to most cellular genes, the transcriptional state of the integrated HIV-I provirus is closely linked to histone acetylation. This enzymatic activity results from the function of histone-specific nuclear acetyltransferase (HAT) enzymes. Efficient viral transcription is strongly dependent on the virally-encoded Tat protein. The mechanism by which Tat increases the rate of transcriptional initiation has been recently demonstrated and involves the interaction of Tat with the transcriptional coactivator p300 and the closely related CREB-binding protein (CBP), having histone acetyltransferase activity

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Authors and Affiliations

  1. International Centre for Genetic Engineering and Biotechnology (ICGEB), Molecular Medicine Laboratory, Padriciano 99, 34012, Trieste, Italy

    Giuseppe Marzio & Mauro Giacca

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  1. Giuseppe Marzio
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  2. Mauro Giacca
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  1. Life Sciences Division, Los Alamos National Laboratory, Los Alamos, New Mexico, USA

    E. Morton Bradbury

  2. Agricultural Biotechnology Centre, Gödöllõ, Hungary

    Sándor Pongor

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Marzio, G., Giacca, M. (1999). Chromatin Control of HIV-1 Gene Expression. In: Bradbury, E.M., Pongor, S. (eds) Structural Biology and Functional Genomics. NATO Science Series, vol 71. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4631-9_13

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  • DOI: https://doi.org/10.1007/978-94-011-4631-9_13

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-0-7923-5782-7

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