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Journal of Virology, November 2004, p. 12198-12206, Vol. 78, No. 22
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.22.12198-12206.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Cell Cycle Arrest in G2 Induces Human Immunodeficiency Virus Type 1 Transcriptional Activation through Histone Acetylation and Recruitment of CBP, NF-{kappa}B, and c-Jun to the Long Terminal Repeat Promoter

Sylvain Thierry,1,2,{dagger} Vincent Marechal,1,2,{dagger} Michelle Rosenzwajg,3 Michèle Sabbah,4 Gérard Redeuilh,4 Jean-Claude Nicolas,2 and Joël Gozlan1,2*

UMR 7079, Université Pierre et Marie Curie,1 UPRES EA 3500, Centre Hospitalier Universitaire Saint-Antoine,2 Laboratoire d'Immunologie et d'Hématologie Biologiques,3 INSERM U482, Hôpital Saint-Antoine, Paris, France4

Received 20 December 2003/ Accepted 29 June 2004

In human immunodeficiency virus type 1 (HIV-1)-infected cells, a cell cycle arrest in G2 increases viral expression and may represent a strategy for the virus to optimize its expression. In latently infected cells, balance between viral silencing and reactivation relies on the nucleosomal organization of the integrated long terminal repeat (LTR). It is shown here that nucleosome nuc-1, which is located downstream of the TATA box, is specifically modified when latently infected cells are arrested in G2 by chemical inducers. Notably, histones H3 and H4 are hyperacetylated, and this modification is associated with an increased LTR-driven transcription. nuc-1 hyperacetylation is also associated with the recruitment of histone acetyltransferase CBP and transcription factors NF-{kappa}B and c-Jun. NF-{kappa}B and/or c-Jun binding to the LTR in G2-arrested cells appears to be required for CBP recruitment as well as for nuc-1 remodeling and viral reactivation.

* Corresponding author. Mailing address: UMR 7079, Université Pierre et Marie Curie, 7 quai Saint-Bernard, 75005, Paris, France. Phone: 33 1 49282936. Fax: 33 1 49282472. E mail: joel.gozlan{at}sat.ap-hop-paris.fr.

{dagger} S.T. and V.M. contributed equally to this work.

Journal of Virology, November 2004, p. 12198-12206, Vol. 78, No. 22
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.22.12198-12206.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.





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