Cocaine-mediated enhancement of virus replication in macrophages: Implications for human immunodeficiency virus-associated dementia.

Cocaine-mediated enhancement of virus replication in macrophages: Implications for human immunodeficiency virus-associated dementia. Research Abstract Details 

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Cocaine-mediated enhancement of virus replication in macrophages: Implications for human immunodeficiency virus-associated dementia. Abstract Text:

Navneet K Dhillon,Rachel Williams,Fuwang Peng,Yi-Jou Tsai,Sukhbir Dhillon,Brandon Nicolay,Milind Gadgil,Anil Kumar,Shilpa J Buch,Navneet K Dhillon,Rachel Williams,Fuwang Peng,Yi-Jou Tsai,Sukhbir Dhillon,Brandon Nicolay,Milind Gadgil,Anil Kumar,Shilpa J Buch,Navneet K Dhillon,Rachel Williams,Fuwang Peng,Yi-Jou Tsai,Sukhbir Dhillon,Brandon Nicolay,Milind Gadgil,Anil Kumar,Shilpa J Buch,

Injection drug use has been recognized as a major risk factor for acquired immunodeficiency syndrome (AIDS) from the outset of the epidemic. Cocaine, one of the most widely abused drugs in the United States, can both impair the functions of macrophages and CD4(+) lymphocytes and also activate human immunodeficiency virus (HIV)-1 expression in these cells. Because the brain is the target organ for both cocaine and HIV, the objective of the present study was to explore the effects of cocaine on virus replication in macrophages, the target cells for the virus in the central nervous system (CNS). Cocaine markedly enhanced virus production in simian human immunodeficiency virus (SHIV)-infected monocyte-derived macrophages (MDMs) and in U1 cells, a chronically infected promonocytic cell line as monitored by enzyme-linked immunosorbent assay (ELISA) and immunocytochemistry. Cocaine treatment also resulted in the activation of nuclear factor (NF)-kappa B and transcriptional activation of the HIV-LTR (long terminal repeat) gag-GFP (green fluorescent protein). Analyses of chemokines in cocaine-treated macrophages by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and Luminex assays suggested increased expression of interleukin (IL)-10, a cytokine that is known to promote HIV replication in MDMs. In addition to enhancing IL-10 expression, cocaine also caused an up-regulation of the macrophage activation marker, human leukocyte antigen (HLA)-DR, in MDMs. The synergistic effect of cocaine on virus replication and its enhancement of host activation markers suggest that cocaine functions at multiple pathways to accelerate HIV-associated dementia (HAD).

Cocaine-mediated enhancement of virus replication in macrophages: Implications for human immunodeficiency virus-associated dementia. Publishing Authors By Initials

NK Dhillon,R Williams,F Peng,YJ Tsai,S Dhillon,B Nicolay,M Gadgil,A Kumar,SJ Buch,NK Dhillon,R Williams,F Peng,YJ Tsai,S Dhillon,B Nicolay,M Gadgil,A Kumar,SJ Buch,NK Dhillon,R Williams,F Peng,YJ Tsai,S Dhillon,B Nicolay,M Gadgil,A Kumar,SJ Buch,

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Cocaine-mediated enhancement of virus replication in macrophages: Implications for human immunodeficiency virus-associated dementia. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Journal of neurovirology

VOLUME: 13

Page Numbers: 483-95

Journal Abbreviation: J. Neurovirol.

ISSN: 1355-0284

DAY: 21

MONTH: Dec

YEAR: 2007

Cocaine-mediated enhancement of virus replication in macrophages: Implications for human immunodeficiency virus-associated dementia. Information

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LANGUAGE: eng

NlmUniqueID: 9508123

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AFFILIATION: Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas, USA.

Country: United States

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MEDLINETA: J Neurovirol

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