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Updated: Oct 13, 2025
Isolation, Transfection, and Culture of Primary Human Monocytes
Published on: December 16, 2019
Methamphetamine facilitates HIV infection of primary human monocytes through inhibiting cellular viral restriction
Yu Liu1, Feng-Zhen Meng1, Xu Wang1,2
1Department of Pathology and Laboratory Medicine, Temple University Lewis Katz School of Medicine, 3500 N Broad St., Philadelphia, PA, 19140, USA.
Background:
Methamphetamine (METH), a potent addictive psychostimulant, is highly prevalent in HIV-infected individuals. Clinically, METH use is implicated in alteration of immune system and increase of HIV spread/replication. Therefore, it is of importance to examine whether METH has direct effect on HIV infection of monocytes, the major target and reservoir cells for the virus.
Results:
METH-treated monocytes were more susceptible to HIV infection as evidenced by increased levels of viral proteins (p24 and Pr55Gag) and expression of viral GAG gene. In addition, using HIV Bal with luciferase reporter gene (HIV Bal-eLuc), we showed that METH-treated cells expressed higher luciferase activities than untreated monocytes. Mechanistically, METH inhibited the expression of IFN-λ1, IRF7, STAT1, and the antiviral IFN-stimulated genes (ISGs: OAS2, GBP5, ISG56, Viperin and ISG15). In addition, METH down-regulated the expression of the HIV restriction microRNAs (miR-28, miR-29a, miR-125b, miR-146a, miR-155, miR-223, and miR-382).
Conclusions:
METH compromises the intracellular anti-HIV immunity and facilitates HIV replication in primary human monocytes.
Insights
Methamphetamine (METH) use increases susceptibility to HIV infection in monocytes by weakening the immune system. This psychostimulant impairs antiviral defenses, facilitating HIV replication in these key cells.
Area of Science:
- Immunology
- Virology
- Neuroscience
Background:
- Methamphetamine (METH) is a prevalent psychostimulant in HIV-infected individuals.
- METH use alters immune function and promotes HIV spread.
- Monocytes are crucial HIV target and reservoir cells.
Purpose of the Study:
- To investigate the direct impact of METH on HIV infection in human monocytes.
Main Methods:
- Monocytes were treated with METH and subsequently infected with HIV.
- Viral protein levels (p24, Pr55Gag) and GAG gene expression were measured.
- Luciferase reporter assays (HIV Bal-eLuc) assessed viral activity.
- Expression of interferon-stimulated genes (ISGs) and HIV restriction microRNAs was analyzed.
Main Results:
- METH-treated monocytes showed increased susceptibility to HIV infection.
- Elevated viral protein and GAG gene expression confirmed higher infection rates.
- METH inhibited key antiviral genes (IFN-λ1, IRF7, STAT1) and ISGs.
- METH down-regulated expression of HIV restriction microRNAs.
Conclusions:
- METH compromises intracellular anti-HIV immunity in monocytes.
- METH facilitates HIV replication in primary human monocytes.
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