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Updated: May 23, 2026
Isolation, Transfection, and Culture of Primary Human Monocytes
Published on: December 16, 2019
Morphine and galectin-1 modulate HIV-1 infection of human monocyte-derived macrophages
Jessica L Reynolds1, Wing Cheung Law, Supriya D Mahajan
1Division of Allergy, Immunology, and Rheumatology, Department of Medicine, State University of New York at Buffalo, Buffalo, NY 14203, USA. jlr8@buffalo.edu
Abstract:
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.
Insights
Morphine increases HIV-1 infection by boosting galectin-1 in macrophages. Nanotechnology using gold nanorods and small interfering RNA (siRNA) successfully reduced galectin-1 and reversed morphine
Area of Science:
- Immunology
- Virology
- Nanotechnology
Background:
- Macrophages are key reservoirs for HIV-1, influencing disease progression.
- Galectin-1, a β-galactoside-binding lectin, mediates cell-pathogen interactions during HIV-1 adhesion.
- Drug abuse and HIV-1 epidemics are interconnected, suggesting potential links between morphine use and HIV-1 infection.
Purpose of the Study:
- To investigate if morphine-induced galectin-1 expression modulates HIV-1 infection in human monocyte-derived macrophages (MDMs).
- To explore the potential of nanotechnology to counteract morphine's effects on galectin-1 and HIV-1 infection.
Main Methods:
- Assessed galectin-1 gene and protein expression in MDMs after morphine incubation.
- Studied the impact of morphine and exogenous galectin-1 on HIV-1 infection rates in MDMs.
- Utilized gold nanorod-galectin-1 small interfering RNA complexes (nanoplexes) to inhibit galectin-1 expression.
Main Results:
- Morphine significantly potentiated galectin-1 gene and protein expression in MDMs.
- Both morphine and galectin-1 alone enhanced HIV-1 infection of MDMs, with combined treatment showing synergistic effects.
- Nanoplexes effectively silenced galectin-1 expression and reversed morphine-induced increases.
- The presence of nanoplexes reduced the enhancing effect of morphine on HIV-1 infection.
Conclusions:
- Morphine potentiates HIV-1 infection in macrophages, at least partly through increased galectin-1 expression.
- Targeting galectin-1 with nanotechnology offers a potential strategy to mitigate the impact of morphine abuse on HIV-1 progression.
- This study highlights the interplay between drug abuse, immune modulation, and viral pathogenesis.
