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Published on: September 5, 2016
Methamphetamine enhances HIV infection of macrophages
1Division of Allergy and Immunology, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Abstract:
Epidemiological studies have demonstrated that the use of methamphetamine (meth), a sympathomimetic stimulant, is particularly common among patients infected with HIV. However, there is a lack of direct evidence that meth promotes HIV infection of target cells. This study examined whether meth is able to enhance HIV infection of macrophages, the primary target site for the virus. Meth treatment resulted in a significant and dose-dependent increase of HIV reverse transcriptase activity in human blood monocyte-derived macrophages. Dopamine D1 receptor antagonists (SCH23390 and SKF83566) blocked this meth-mediated increase in the HIV infectivity of macrophages. Investigation of the underlying mechanisms of meth action showed that meth up-regulated the expression of the HIV entry co-receptor CCR5 on macrophages. Additionally, meth inhibited the expression of endogenous interferon-alpha and signal transducer and activator of transcription-1 in macrophages. These findings provide direct in vitro evidence to support the possibility that meth may function as a cofactor in the immunopathogenesis of HIV infection and may lead to the future development of innate immunity-based intervention for meth users with HIV infection.
Insights
Methamphetamine use significantly increases HIV infection in macrophages, the primary target cells. This stimulant may act as a cofactor in HIV pathogenesis, suggesting new intervention strategies for HIV-positive individuals using meth.
Area of Science:
- Immunology
- Virology
- Neuroscience
Background:
- Methamphetamine (meth) use is prevalent in HIV-infected individuals.
- Direct evidence linking meth to enhanced HIV infection is lacking.
- Macrophages are a primary target for HIV infection.
Purpose of the Study:
- To investigate if meth enhances HIV infection in macrophages.
- To explore the mechanisms behind meth's effect on HIV infectivity.
- To identify potential therapeutic targets for HIV-infected meth users.
Main Methods:
- Human blood monocyte-derived macrophages were treated with varying doses of meth.
- HIV reverse transcriptase activity was measured to assess infection levels.
- Dopamine D1 receptor antagonists were used to block meth's effects.
- Expression of HIV co-receptor CCR5 and immune mediators (interferon-alpha, STAT-1) was analyzed.
Main Results:
- Meth significantly increased HIV reverse transcriptase activity in a dose-dependent manner.
- Dopamine D1 receptor antagonists reversed the meth-induced increase in HIV infectivity.
- Meth upregulated CCR5 expression on macrophages.
- Meth inhibited endogenous interferon-alpha and STAT-1 expression.
Conclusions:
- Meth directly enhances HIV infection of macrophages in vitro.
- Meth may act as a cofactor in HIV immunopathogenesis.
- Findings suggest potential for innate immunity-based interventions for HIV-infected meth users.
