Morphine stimulates HIV replication in primary cultures of human Kupffer cells

Schweitzer, Christine; Keller, F.; Schmitt, Marie-Paule; Jaeck, Daniel; Adloff, M; Schmitt, Carine; Royer, Corinne; Kirn, A.; Aubertin, Anne-Marie

doi:10.1016/0923-2516(91)90056-9

Cited by 44 publications

(24 citation statements)

References 19 publications

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“…Morphine amplifies HIV-1 expression in the chronically infected promonocytic clone U1 when cocultured with lipopolysaccharide-stimulated human fetal brain cells (46). Morphine stimulated HIV-1 replication in primary cultures of human Kupffer cells (47). Morphine significantly enhanced HIV-1 R5 strain infection of MDM but had little effect on X4 strain infection (5).…”

Section: Discussionmentioning

confidence: 99%

Morphine and Galectin-1 Modulate HIV-1 Infection of Human Monocyte-Derived Macrophages

Reynolds

Law

Mahajan

et al. 2012

The Journal of Immunology

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Morphine is a widely abused, addictive drug that modulates immune function. Macrophages are a primary reservoir of HIV-1; therefore, they play a role in the development of this disease, as well as impact the overall course of disease progression. Galectin-1 is a member of a family of β-galactoside–binding lectins that are soluble adhesion molecules and that mediate direct cell–pathogen interactions during HIV-1 viral adhesion. Because the drug abuse epidemic and the HIV-1 epidemic are closely interrelated, we propose that increased expression of galectin-1 induced by morphine may modulate HIV-1 infection of human monocyte-derived macrophages (MDMs). In this article, we show that galectin-1 gene and protein expression are potentiated by incubation with morphine. Confirming previous studies, morphine alone or galectin-1 alone enhance HIV-1 infection of MDMs. Concomitant incubation with exogenous galectin-1 and morphine potentiated HIV-1 infection of MDMs. We used a nanotechnology approach that uses gold nanorod–galectin-1 small interfering RNA complexes (nanoplexes) to inhibit gene expression for galectin-1. We found that nanoplexes silenced gene expression for galectin-1, and they reversed the effects of morphine on galectin-1 expression. Furthermore, the effects of morphine on HIV-1 infection were reduced in the presence of the nanoplex.

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Section: Discussionmentioning

confidence: 99%

Morphine and Galectin-1 Modulate HIV-1 Infection of Human Monocyte-Derived Macrophages

Reynolds

Law

Mahajan

et al. 2012

The Journal of Immunology

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“…Opioids are widely prescribed and also abused drugs in the United States and all over the world. Several studies from different laboratories indicate that opioid use may promote HIV disease progression by enhancing HIV replication and infection (Peterson et al 1990;Schweitzer et al 1991;Suzuki et al 2002;Guo et al 2002;Li et al 2003;Ho et al 2003;Wang et al 2005). Opoids, especially morphine, has been shown to promote HIV replication in many cell types through various mechanisms which are described below.…”

Section: Effect Of Morphine On Anti-hiv Mirna Expression In Monocytesmentioning

confidence: 99%

Do Opioids Activate Latent HIV-1 by Down-Regulating Anti-HIV microRNAs?

Purohit

Rapaka

Rutter

et al. 2012

J Neuroimmune Pharmacol

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“…Morphine stimulates the replication of the HIV virus [99], and may accelerate progression to AIDS [100]. Opiate misuse also seems to increase rates of symptomatic illness in people with HIV [101].…”

Section: Neuropsychology Of Hiv and Aidsmentioning

confidence: 99%

Neuropsychological Consequences of HIV and Substance Abuse: A Literature Review and Implications for Treatment and Future Research

Norman¹,

Basso²,

Kumar³

et al. 2009

CDAR

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Neuropsychological dysfunction, ranging from mild cognitive symptoms to dementia has been a consistent part of the clinical picture of HIV/AIDS. However, advances in clinical management, particularly antiretroviral (ARV) treatment, have mitigated the neuropsychological effects of HIV and revised the pattern and nature of cognitive deficits, which are observed in HIV-infected individuals. The attendant improvements in mortality and morbidity have led to a need for programs and interventions that sustain healthy behavior and prevent a resurgence of HIV transmission risk. Psychiatric risk factors, particularly substance use, which often contribute to initial acquisition of HIV, still require attention. These risk factors may also exacerbate neuropsychological dysfunction and compromise adherence to prevention recommendations and treatment. Specifically, a more complete understanding of the effects of substance abuse on the progression of HIV related cognitive decline can inform evaluation and management of HIV seropositives with concurrent substance use disorders. This review provides an overview of the neuropsychology of HIV and substance abuse and the extant research that has examined the effects of both HIV disease and substance use on neuropsychological functioning and implications for treatment and future research.

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Morphine stimulates HIV replication in primary cultures of human Kupffer cells

Cited by 44 publications

References 19 publications

Morphine and Galectin-1 Modulate HIV-1 Infection of Human Monocyte-Derived Macrophages

Morphine and Galectin-1 Modulate HIV-1 Infection of Human Monocyte-Derived Macrophages

Do Opioids Activate Latent HIV-1 by Down-Regulating Anti-HIV microRNAs?

Neuropsychological Consequences of HIV and Substance Abuse: A Literature Review and Implications for Treatment and Future Research

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