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Isolation, Transfection, and Culture of Primary Human Monocytes
Published on: December 16, 2019
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HIV-1 latency in monocytes/macrophages
Amit Kumar1, Wasim Abbas2, Georges Herbein3
1UPRES EA4266, SFR FED 4234, Pathogens and Inflammation Laboratory, Department of Virology, CHRU Besançon, University of Franche-Comte, F-25030 Besançon, France. amit.aiims2005@gmail.com.
Viruses
|April 25, 2014
Summary
Human immunodeficiency virus type 1 (HIV-1) establishes latent reservoirs in monocyte/macrophage lineage cells, which are crucial for a complete HIV cure. Targeting these persistent viral hideouts is essential for eradicating HIV-1 infection.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Human immunodeficiency virus type 1 (HIV-1) infects CD4+ T cells and monocyte/macrophage lineage cells.
- HIV pathogenesis involves T cell depletion and the establishment of latent viral reservoirs.
- While highly active antiretroviral therapy (HAART) improves patient outcomes, it cannot eliminate latent HIV-1 reservoirs.
Purpose of the Study:
- To review the current understanding of HIV-1 latency mechanisms within the monocyte/macrophage lineage.
- To explore strategies for the specific elimination of these neglected latent HIV-1 reservoirs.
Main Methods:
- Review of existing scientific literature on HIV-1 latency.
- Analysis of the role of monocyte/macrophage lineage cells in HIV-1 persistence.
- Discussion of potential therapeutic targets for eliminating latent reservoirs.
Main Results:
- HIV-1 establishes latency not only in resting CD4+ T cells but also in monocyte/macrophage lineage cells (monocytes, macrophages, brain resident macrophages).
- These cells are more resistant to HIV-1-induced apoptosis, serving as stable viral reservoirs.
- Current efforts to eradicate HIV-1 have largely overlooked these monocyte/macrophage reservoirs.
Conclusions:
- Eliminating latent HIV-1 reservoirs in the monocyte/macrophage lineage is critical for achieving a functional cure for HIV-1.
- Further research into the mechanisms of latency in these cells and the development of targeted elimination strategies are necessary.

