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Updated: Jan 13, 2026
Phagosome Migration and Velocity Measured in Live Primary Human Macrophages Infected with HIV-1
Published on: September 5, 2016
Endogenous HIV-1 Tat Promotes Cell Proliferation, Migration, and Phagocytosis in Stably Infected Macrophages by
Yang Wei-Ling1,2,3, Xiao Na1,2,3, Liu Lin1,2,3
1Graduate School, Youjiang Medical University for Nationalities, Baise, Guangxi, China.
Abstract:
HIV-1 infection remains difficult to treat due to the virus's ability to persist in host cells such as memory CD4+ T cells and peripheral macrophages. Tat, an HIV-1 regulatory protein, also modulates transcription in host cells. However, the mechanisms by which Tat stably affects macrophage functions, critical host cells for HIV-1, remain unclear. This study demonstrates that Tat promotes macrophage proliferation, migration, and phagocytosis. In-depth analysis reveals that HIV-1 Tat enhances lactate accumulation, induces reactive oxygen species (ROS), and activates the MAPK pathway in macrophages. Additionally, lactate induces autophagy activation, leading to increased levels of Arg1 and TGF-β, which drive phagocytosis and migration, respectively. By examining the activity of macrophages stably infected with Tat, this study provides new insights into Tat's latent influence on macrophage function, offering theoretical support for understanding HIV-1 infection mechanisms.
Insights
HIV-1 Tat protein enhances macrophage functions like proliferation and migration. It achieves this by increasing lactate, reactive oxygen species, and activating the MAPK pathway, offering insights into HIV-1 persistence.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- HIV-1 infection is challenging due to viral persistence in macrophages and CD4+ T cells.
- The HIV-1 Tat protein's role in stably altering macrophage function is not fully understood.
Purpose of the Study:
- To investigate the mechanisms by which HIV-1 Tat influences macrophage functions.
- To elucidate Tat's impact on macrophage proliferation, migration, and phagocytosis.
Main Methods:
- Analysis of macrophage proliferation, migration, and phagocytosis.
- Measurement of lactate accumulation, reactive oxygen species (ROS) production, and MAPK pathway activation.
- Investigation of autophagy activation and downstream effects of lactate.
Main Results:
- HIV-1 Tat significantly promotes macrophage proliferation, migration, and phagocytosis.
- Tat enhances lactate accumulation, ROS production, and MAPK pathway activation in macrophages.
- Lactate induces autophagy, increasing Arg1 and TGF-β levels, which mediate phagocytosis and migration.
Conclusions:
- HIV-1 Tat exerts a latent influence on macrophage functions, promoting key activities.
- The study reveals a novel pathway involving lactate, ROS, MAPK, and autophagy in Tat-mediated macrophage modulation.
- Findings offer theoretical support for understanding HIV-1 infection and persistence mechanisms.
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