Morphine and galectin-1 modulate HIV-1 infection of human monocyte-derived macrophages

Jessica L. Reynolds, Wing Cheung Law, Supriya D. Mahajan, Ravikumar Aalinkeel, Bindukumar Nair, Donald E. Sykes, Manoj J. Mammen, Ken Tye Yong, Rui Hui, Paras N. Prasad, Stanley A. Schwartz

Research output: Journal article publicationJournal articleAcademic researchpeer-review

26 Citations (Scopus)


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.
Original languageEnglish
Pages (from-to)3757-3765
Number of pages9
JournalJournal of Immunology
Issue number8
Publication statusPublished - 15 Apr 2012
Externally publishedYes

ASJC Scopus subject areas

  • Immunology


Dive into the research topics of 'Morphine and galectin-1 modulate HIV-1 infection of human monocyte-derived macrophages'. Together they form a unique fingerprint.

Cite this