Cocaine and HIV-1 Interplay in CNS: Cellular and Molecular Mechanisms
Shilpa Buch, Honghong Yao, Minglei Guo, Tomohisa Mori, Blaise Mathias-Costa, Vijeta Singh, Pankaj Seth, John Wang and Tsung-Ping Su
Affiliation: Department of Pharmacology and Experimental Neuroscience, 985880 Nebraska Medical Center (DRC 8011), University of Nebraska Medical Center, Omaha, NE 68198-5880, USA.
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.
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