This is a powerful pathogenic strategy that could favor cell-to-cell spreading of the virus by inhibiting T cell migration in lymph nodes and promoting virus dissemination through body tissues by enhancing macrophage 3D mesenchymal migration. Similarly to the actin-based motility of bacteria employed by Listeria or Shigella , a biological context that yielded major advances in the in-depth knowledge of the actin polymerization machinery 66 , HIV-1 has similarly developed a strategy to exploit the actin cytoskeleton and cell migration, and this way, reveals substantial insights into molecular pathways regulating cell migration.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. We greatly acknowledge the TRI imaging platform, S. Souriant for figure preparation and A. Lugo-Villarino for critical reading of the manuscript.
- HIV-1 Infection of T Lymphocytes and Macrophages Affects Their Migration via Nef.
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National Center for Biotechnology Information , U. Journal List Front Immunol v.
Published online Oct 6. Received Jun 9; Accepted Sep The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. This article has been cited by other articles in PMC. Abstract The human immunodeficiency virus HIV-1 disseminates in the body and is found in several organs and tissues. Introduction The biology and pathogenesis of HIV infection has been largely studied since the discovery of the virus in Open in a separate window.
A Potential Pharmacological Target Nef modulates the function of several proteins also described to localize at podosomes, including Wiskott—Aldrich syndrome protein WASP , Hck, paxillin, and cofilin 18 , 51 — A Promising Pharmacological Target to Limit Macrophage Tissue Infiltration Although macrophages play a key role in immune protection, they also play detrimental roles in several diseases including cancer and chronic inflammations.
Conclusion HIV-1 is able to modify the migration of its main host cells T lymphocytes and macrophages via Nef, which appears as a key regulator of the migration of T cells and the different modes of macrophage migration.
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Conflict of Interest Statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Nat Rev Microbiol Cell Host Microbe Cell-to-cell transfer of HIV infection: J Gen Virol Broadly neutralizing antibodies that inhibit HIV-1 cell to cell transmission. J Exp Med Nat Rev Microbiol 6: Nat Immunol HIV-infected T cells are migratory vehicles for viral dissemination.
HIV-1 reprograms the migration of macrophages. HIV-1 gp chemokine receptor-mediated signaling in human macrophages.
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Immunol Res Viral Immunol The regulation of alpha chemokines during HIV-1 infection and leukocyte activation: J Neuroimmunol HIV-1 Nef mediates lymphocyte chemotaxis and activation by infected macrophages. Nat Med 5: Nonmuscle myosin light-chain kinase mediates microglial migration induced by HIV tat: HIV Nef inhibits T cell migration. J Biol Chem M [ PubMed ] [ Cross Ref ]. HIV-1 Nef inhibits ruffles, induces filopodia, and modulates migration of infected lymphocytes.
J Virol HIV-1 Nef-mediated inhibition of T cell migration and its molecular determinants. J Leukoc Biol HIV-1 Nef interferes with T-lymphocyte circulation through confined environments in vivo. HIV-1 Nef interferes with host cell motility by deregulation of cofilin. Cell Host Microbe 6: Cell Rep 7: Matrix architecture dictates three-dimensional migration modes of human macrophages: J Immunol J Cell Sci Protrusion force microscopy reveals oscillatory force generation and mechanosensing activity of human macrophage podosomes.
Nat Commun 5: Podosomes are disrupted in PAPA syndrome. Control of macrophage 3D migration: Immunol Rev An efficient siRNA-mediated gene silencing in primary human monocytes, dendritic cells and macrophages. Immunol Cell Biol 92 8: Cell Adh Migr 8 3: Macrophage podosomes go 3D. Eur J Cell Biol Blood leukocytes and macrophages of various phenotypes have distinct abilities to form podosomes and to migrate in 3D environments. The cellular and molecular origin of tumor-associated macrophages.
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