PMID- 18097880
OWN - NLM
STAT- MEDLINE
DCOM- 20080328
LR  - 20211020
IS  - 1355-0284 (Print)
IS  - 1355-0284 (Linking)
VI  - 13
IP  - 6
DP  - 2007 Dec
TI  - Cocaine-mediated enhancement of virus replication in macrophages: implications 
      for human immunodeficiency virus-associated dementia.
PG  - 483-95
AB  - 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).
FAU - Dhillon, Navneet K
AU  - Dhillon NK
AD  - Department of Molecular and Integrative Physiology, University of Kansas Medical 
      Center, Kansas City, Kansas 66160, USA.
FAU - Williams, Rachel
AU  - Williams R
FAU - Peng, Fuwang
AU  - Peng F
FAU - Tsai, Yi-Jou
AU  - Tsai YJ
FAU - Dhillon, Sukhbir
AU  - Dhillon S
FAU - Nicolay, Brandon
AU  - Nicolay B
FAU - Gadgil, Milind
AU  - Gadgil M
FAU - Kumar, Anil
AU  - Kumar A
FAU - Buch, Shilpa J
AU  - Buch SJ
LA  - eng
GR  - DA020392-01/DA/NIDA NIH HHS/United States
GR  - MH-068212/MH/NIMH NIH HHS/United States
GR  - MH072355/MH/NIMH NIH HHS/United States
GR  - MH62969-01/MH/NIMH NIH HHS/United States
GR  - RR016443/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Neurovirol
JT  - Journal of neurovirology
JID - 9508123
RN  - 147336-22-9 (Green Fluorescent Proteins)
RN  - I5Y540LHVR (Cocaine)
SB  - IM
MH  - AIDS Dementia Complex/*etiology/pathology
MH  - Acquired Immunodeficiency Syndrome
MH  - Animals
MH  - Cocaine/*pharmacology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Green Fluorescent Proteins
MH  - HIV/*physiology
MH  - HIV Infections/*complications/immunology
MH  - HIV Long Terminal Repeat
MH  - Humans
MH  - Macaca mulatta
MH  - Macrophages/metabolism/*virology
MH  - Virus Replication/*drug effects
EDAT- 2007/12/22 09:00
MHDA- 2008/03/29 09:00
CRDT- 2007/12/22 09:00
PHST- 2007/12/22 09:00 [pubmed]
PHST- 2008/03/29 09:00 [medline]
PHST- 2007/12/22 09:00 [entrez]
AID - 788723927 [pii]
AID - 10.1080/13550280701528684 [doi]
PST - ppublish
SO  - J Neurovirol. 2007 Dec;13(6):483-95. doi: 10.1080/13550280701528684.