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Phagosome Migration and Velocity Measured in Live Primary Human Macrophages Infected with HIV-1
Published on: September 5, 2016
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HIV-1 reprograms the migration of macrophages
Christel Vérollet1, Shanti Souriant1, Emilie Bonnaud1
1Centre National de la Recherche Scientifique Unité Mixte de Recherche 5089, Institut de Pharmacologie et de Biologie Structurale, Toulouse Cedex 04, France; Université de Toulouse-Paul Sabatier, Institut de Pharmacologie et de Biologie Structurale, Toulouse, France;
Blood
|December 21, 2014
Summary
Human immunodeficiency virus type 1 (HIV-1) infection alters macrophage migration. The viral protein Nef enhances mesenchymal migration, increasing tissue infiltration and contributing to disease.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Macrophages are key immune cells targeted by HIV-1.
- Their role in viral dissemination is established, but migration changes post-infection are unclear.
Purpose of the Study:
- To investigate the impact of HIV-1 infection on macrophage migration capacity.
- To identify the viral mechanisms responsible for altered migration.
Main Methods:
- Studied migration modes (2D, 3D amoeboid, 3D mesenchymal) of HIV-1-infected macrophages.
- Utilized Nef transgenic mice to assess in vivo tissue infiltration.
- Investigated podosome dynamics and signaling pathways (Hck, WASP).
Main Results:
- HIV-1 infection inhibited 2D and 3D amoeboid migration but enhanced 3D mesenchymal migration.
- The viral protein Nef mediated these migration changes.
- Nef increased macrophage tissue infiltration in mice, linked to enhanced mesenchymal motility, podosome stability, and Hck/WASP signaling.
Conclusions:
- HIV-1 reprograms macrophage migration, promoting mesenchymal motility.
- This reprogramming likely contributes to macrophage accumulation in tissues, aiding virus spread and pathogenesis.
- Nef, podosomes, and the Hck/WASP pathway are key regulators of macrophage tissue infiltration relevant to HIV-1 and other diseases.
