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Role of mu-opioids as cofactors in human immunodeficiency virus type 1 disease progression and neuropathogenesis
Journal article   Open access   Peer reviewed

Role of mu-opioids as cofactors in human immunodeficiency virus type 1 disease progression and neuropathogenesis

Anupam Banerjee, Marianne Strazza, Brian Wigdahl, Vanessa Pirrone, Olimpia Meucci and Michael R Nonnemacher
Journal of neurovirology, v 17(4), pp 291-302
Aug 2011
PMID: 21735315
url
https://doi.org/10.1007/s13365-011-0037-2View
Published, Version of Record (VoR) Open

Abstract

HIV-1 Cyclic AMP (cAMP) Opioids
About one third of acquired immunodeficiency syndrome cases in the USA have been attributed to the use of injected addictive drugs, frequently involving opioids like heroin and morphine, establishing them as significant predisposing risk factors for contracting human immuno-deficiency virus type 1 (HIV-1). Accumulating evidence from in vitro and in vivo experimental systems indicates that opioids act in concert with HIV-1 proteins to exacerbate dysregulation of neural and immune cell function and survival through diverse molecular mechanisms. In contrast, the impact of opioid exposure and withdrawal on the viral life cycle and HIV-1 disease progression itself is unclear, with conflicting reports emerging from the simian immunodeficiency virus and simian–human immunodeficiency virus infection models. However, these studies suggest a potential role of opioids in elevated viral production. Because human microglia, astrocytes, CD4+ T lymphocytes, and monocyte-derived macrophages express opioid receptors, it is likely that intracellular signaling events triggered by morphine facilitate enhancement of HIV-1 infection in these target cell populations. This review highlights the biochemical changes that accompany prolonged exposure to and withdrawal from morphine that synergize with HIV-1 proteins to disrupt normal cellular physiological functions especially within the central nervous system. More importantly, it collates evidence from epidemiological studies, animal models, and heterologous cell systems to propose a mechanistic link between such physiological adaptations and direct modulation of HIV-1 production. Understanding the opioid–HIV-1 interface at the molecular level is vitally important in designing better treatment strategies for HIV-1-infected patients who abuse opioids.

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Web of Science research areas
Neurosciences
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