Abstract
Although antiretrovirals are the mainstay of therapy against HIV infection, neurological complications associated with the virus continue to hamper quality of life of the infected individuals. Drugs of abuse in the infected individuals further fuel the epidemic. Epidemiological studies have demonstrated that abuse of cocaine resulted in acceleration of HIV infection and the progression of NeuroAIDS. Cocaine has not only been shown to play a crucial role in promoting virus replication, but also has diverse but often deleterious effects on various cell types of the CNS. In the neuronal system, cocaine exposure results in neuronal toxicity and also potentiates gp120-induced neurotoxicity. In the astroglia and microglia, cocaine exposure leads to up-regulation of pro-inflammatory mediators such as cytokines and chemokines. These in turn, can lead to neuroinflammation and transmission of toxic responses to the neurons. Additionally, cocaine exposure can also lead to leakiness of the blood-brain barrier that manifests as enhanced transmigraiton of leukocytes/monocytes into the CNS. Both in vitro and in vivo studies have provided valuable tools in exploring the role of cocaine in mediating HIV-associated neuropathogenesis. This review summarizes previous studies on the mechanism(s) underlying the interplay of cocaine and HIV as it relates to the CNS.
Keywords: HIV, AIDS, cocaine, Glial cell, neuron, HIV-1-associated neurocognitive disorders, NMDA receptor, CNS, non-opioid receptor, HAND.
Current HIV Research
Title:Cocaine and HIV-1 Interplay in CNS: Cellular and Molecular Mechanisms
Volume: 10 Issue: 5
Author(s): Shilpa Buch, Honghong Yao, Minglei Guo, Tomohisa Mori, Blaise Mathias-Costa, Vijeta Singh, Pankaj Seth, John Wang and Tsung-Ping Su
Affiliation:
Keywords: HIV, AIDS, cocaine, Glial cell, neuron, HIV-1-associated neurocognitive disorders, NMDA receptor, CNS, non-opioid receptor, HAND.
Abstract: Although antiretrovirals are the mainstay of therapy against HIV infection, neurological complications associated with the virus continue to hamper quality of life of the infected individuals. Drugs of abuse in the infected individuals further fuel the epidemic. Epidemiological studies have demonstrated that abuse of cocaine resulted in acceleration of HIV infection and the progression of NeuroAIDS. Cocaine has not only been shown to play a crucial role in promoting virus replication, but also has diverse but often deleterious effects on various cell types of the CNS. In the neuronal system, cocaine exposure results in neuronal toxicity and also potentiates gp120-induced neurotoxicity. In the astroglia and microglia, cocaine exposure leads to up-regulation of pro-inflammatory mediators such as cytokines and chemokines. These in turn, can lead to neuroinflammation and transmission of toxic responses to the neurons. Additionally, cocaine exposure can also lead to leakiness of the blood-brain barrier that manifests as enhanced transmigraiton of leukocytes/monocytes into the CNS. Both in vitro and in vivo studies have provided valuable tools in exploring the role of cocaine in mediating HIV-associated neuropathogenesis. This review summarizes previous studies on the mechanism(s) underlying the interplay of cocaine and HIV as it relates to the CNS.
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Cite this article as:
Buch Shilpa, Yao Honghong, Guo Minglei, Mori Tomohisa, Mathias-Costa Blaise, Singh Vijeta, Seth Pankaj, Wang John and Su Tsung-Ping, Cocaine and HIV-1 Interplay in CNS: Cellular and Molecular Mechanisms, Current HIV Research 2012; 10 (5) . https://dx.doi.org/10.2174/157016212802138823
DOI https://dx.doi.org/10.2174/157016212802138823 |
Print ISSN 1570-162X |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4251 |
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