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Cocaine accelerates human immunodeficiency virus (HIV-1) replication by altering specific cell-signaling and epigenetic pathways. We have elucidated the underlying molecular mechanisms through which cocaine exerts its effect in myeloid cells, a major target of HIV-1 in central nervous system (CNS). We demonstrate that cocaine treatment promotes HIV-1 gene expression by activating both nuclear factor-kappa B (NF-ĸB) and mitogen- and stress-activated kinase 1 (MSK1). MSK1 subsequently catalyzes the phosphorylation of histone H3 at serine 10, and p65 subunit of NF-ĸB at 276th serine residue. These modifications enhance the interaction of NF-ĸB with P300 and promote the recruitment of the positive transcription elongation factor b (P-TEFb) to the HIV-1 LTR, supporting the development of an open/relaxed chromatin configuration, and facilitating the initiation and elongation phases of HIV-1 transcription. Results are also confirmed in primary monocyte derived macrophages (MDM). Overall, our study provides detailed insights into cocaine-driven HIV-1 transcription and replication.

Titel:	Cocaine promotes both initiation and elongation phase of HIV-1 transcription by activating NF-κB and MSK1 and inducing selective epigenetic modifications at HIV-1 LTR.
Autor/in / Beteiligte Person:	Sahu, G ; Farley, K ; El-Hage, N ; Aiamkitsumrit, B ; Fassnacht, R ; Kashanchi, F ; Ochem, A ; Simon, GL ; Karn, J ; Hauser, KF ; Tyagi, M
Link:	Full Text Finder (Volltext)
Zeitschrift:	Virology, Jg. 483 (2015-09-01), S. 185-202
Veröffentlichung:	New York, Academic Press., 2015
Medientyp:	academicJournal
ISSN:	1096-0341 (electronic)
DOI:	10.1016/j.virol.2015.03.036
Schlagwort:	Cells, Cultured HIV Long Terminal Repeat Humans Macrophages drug effects Macrophages virology Monocytes drug effects Monocytes virology Cocaine metabolism Epigenesis, Genetic drug effects HIV-1 drug effects NF-kappa B metabolism Ribosomal Protein S6 Kinases, 90-kDa metabolism Transcription, Genetic drug effects
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Language: English [Virology] 2015 Sep; Vol. 483, pp. 185-202. <i>Date of Electronic Publication: </i>2015 May 15. MeSH Terms: Cocaine / metabolism ; Epigenesis, Genetic / drug effects ; HIV-1 / drug effects ; NF-kappa B / metabolism ; Ribosomal Protein S6 Kinases, 90-kDa / metabolism ; Transcription, Genetic / drug effects ; Cells, Cultured ; HIV Long Terminal Repeat ; Humans ; Macrophages / drug effects ; Macrophages / virology ; Monocytes / drug effects ; Monocytes / virology References: Biochem J. 2005 Apr 15;387(Pt 2):507-17. (PMID: 15568999) ; EMBO J. 1994 Oct 3;13(19):4597-607. (PMID: 7925300) ; EMBO J. 2003 Mar 17;22(6):1313-24. (PMID: 12628924) ; Ann N Y Acad Sci. 2007 Dec;1122:144-54. (PMID: 18077570) ; Nature. 2013 Jun 20;498(7454):305-6. (PMID: 23739334) ; J Antimicrob Chemother. 2006 May;57(5):803-5. 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(PMID: 16339038) Grant Information: P30 AI087714 United States AI NIAID NIH HHS; K02 DA027374 United States DA NIDA NIH HHS; R01 AI043894 United States AI NIAID NIH HHS; R01DA033200 United States DA NIDA NIH HHS; 5R03DA033900-02 United States DA NIDA NIH HHS; R01 DA033200 United States DA NIDA NIH HHS; 5P30AI087714-02 United States AI NIAID NIH HHS; R03 DA033900 United States DA NIDA NIH HHS; 5R21DA033924-02 United States DA NIDA NIH HHS; K02DA027374 United States DA NIDA NIH HHS; R21 DA033924 United States DA NIDA NIH HHS Contributed Indexing: Keywords: Chromatin; Cocaine; Elongation; H3; HIV-1; MSK1; NF-ĸB; RSK1; Transcription; p65 Substance Nomenclature: 0 (NF-kappa B) ; EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 90-kDa) ; EC 2.7.11.1 (mitogen and stress-activated protein kinase 1) ; I5Y540LHVR (Cocaine) Entry Date(s): Date Created: 20150519 Date Completed: 20151012 Latest Revision: 20181113 Update Code: 20231215 PubMed Central ID: PMC4516702

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Cocaine promotes both initiation and elongation phase of HIV-1 transcription by activating NF-κB and MSK1 and inducing selective epigenetic modifications at HIV-1 LTR.