Generic placeholder image

Current HIV Research

Editor-in-Chief

ISSN (Print): 1570-162X
ISSN (Online): 1873-4251

Cocaine and HIV-1 Interplay in CNS: Cellular and Molecular Mechanisms

Author(s): Shilpa Buch, Honghong Yao, Minglei Guo, Tomohisa Mori, Blaise Mathias-Costa, Vijeta Singh, Pankaj Seth, John Wang and Tsung-Ping Su

Volume 10, Issue 5, 2012

Page: [425 - 428] Pages: 4

DOI: 10.2174/157016212802138823

Price: $65

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.


Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy