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1. Robust Control of a Brain-Persisting Parasite through MHC I Presentation by Infected Neurons

Author

Salvioni, Anna, Belloy, Marcy, Lebourg, Aurore, Bassot, Emilie, Cantaloube-Ferrieu, Vincent, Vasseur, Virginie, Blanié, Sophie, Liblau, Roland S, Suberbielle, Elsa, Robey, Ellen A, and Blanchard, Nicolas

Subjects
Biological Sciences, Neurosciences, Emerging Infectious Diseases, Infectious Diseases, Biodefense, Brain Disorders, Prevention, Vaccine Related, Infection, Neurological, Animals, Antibodies, Protozoan, Antigens, Protozoan, Brain, Cell Line, Cells, Cultured, Histocompatibility Antigens Class I, Humans, Male, Mice, Mice, Inbred C57BL, Neurons, Protozoan Proteins, Toxoplasma, Toxoplasmosis, Cerebral, CD8 T cell, Toxoplasma gondii, antigen presentation, brain infection, encephalitis, neuroinflammation, neuron, parasite, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract

Control of CNS pathogens by CD8 T cells is key to avoid fatal neuroinflammation. Yet, the modalities of MHC I presentation in the brain are poorly understood. Here, we analyze the antigen presentation mechanisms underlying CD8 T cell-mediated control of the Toxoplasma gondii parasite in the CNS. We show that MHC I presentation of an efficiently processed model antigen (GRA6-OVA), even when not expressed in the bradyzoite stage, reduces cyst burden and dampens encephalitis in C57BL/6 mice. Antigen presentation assays with infected primary neurons reveal a correlation between lower MHC I presentation of tachyzoite antigens by neurons and poor parasite control in vivo. Using conditional MHC I-deficient mice, we find that neuronal MHC I presentation is required for robust restriction of T. gondii in the CNS during chronic phase, showing the importance of MHC I presentation by CNS neurons in the control of a prevalent brain pathogen.

Published
2019

2. Productive HIV-1 infection of tissue macrophages by fusion with infected CD4+ T cells

Author

Mascarau, Rémi, primary, Woottum, Marie, additional, Fromont, Léa, additional, Gence, Rémi, additional, Cantaloube-Ferrieu, Vincent, additional, Vahlas, Zoï, additional, Lévêque, Kevin, additional, Bertrand, Florent, additional, Beunon, Thomas, additional, Métais, Arnaud, additional, El Costa, Hicham, additional, Jabrane-Ferrat, Nabila, additional, Gallois, Yohan, additional, Guibert, Nicolas, additional, Davignon, Jean-Luc, additional, Favre, Gilles, additional, Maridonneau-Parini, Isabelle, additional, Poincloux, Renaud, additional, Lagane, Bernard, additional, Bénichou, Serge, additional, Raynaud-Messina, Brigitte, additional, and Vérollet, Christel, additional

Published
2023
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3. Targeting APC-Host Microbe interactions 2Robust control of a neurotropic parasite through MHC I presentation by infected neurons

Author

Salvioni, Anna, primary, Belloy, Marcy, additional, Lebourg, Aurore, additional, Bassot, Emilie, additional, Cantaloube-Ferrieu, Vincent, additional, Vasseur, Virginie, additional, Blanié, Sophie, additional, Liblau, Roland S., additional, Suberbielle, Elsa, additional, Robey, Ellen A., additional, and Blanchard, Nicolas, additional

Published
2022
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5. Mechanisms of HIV-1 evasion to the antiviral activity of chemokine CXCL12 indicate potential links with pathogenesis

Author

Armani-Tourret, Marie, Zhou, Zhicheng, Gasser, Romain, Staropoli, Isabelle, Cantaloube-Ferrieu, Vincent, Benureau, Yann, Garcia-Perez, Javier, Pérez-Olmeda, Mayte, Lorin, Valérie, Puissant-Lubrano, Bénédicte, Assoumou, Lambert, Delaugerre, Constance, Lelièvre, Jean-Daniel, Lévy, Yves, Mouquet, Hugo, Martin-Blondel, Guillaume, Alcami, Jose, Arenzana-Seisdedos, Fernando, Izopet, Jacques, Colin, Philippe, Lagane, Bernard, Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Pathogénie Virale, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Instituto de Salud Carlos III [Madrid] (ISC), Immunologie humorale - Humoral Immunology, Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Génomes, biologie cellulaire et thérapeutiques (GenCellDi (UMR_S_944)), Collège de France (CdF (institution))-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), CHU Henri Mondor, Service des maladies infectieuses et tropicales [Toulouse], Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse], Laboratoire de Virologie [Toulouse], This work was supported by Agence Nationale de Recherches sur le SIDA et les hépatites virales (ANRS) (http://www.anrs.fr/fr) (Grants AAP-2013-2 and ECTZ63419 to B.L.), Institut National de la Santé et de la Recherche Médicale (INSERM) (https://www.inserm.fr), Institut Pasteur (https://www.pasteur.fr), Université Paul Sabatier Toulouse III (https://www.univ-tlse3.fr), The Milieu Intérieur Program (ANR-10-LABX-69-01 to H.M.) (http://www.milieuinterieur.fr) and Instituto de Salud Carlos III (projects RD16CIII/0002/0001 and PI19CIIII/0004 to J.A.) (https://www.isciii.es). M.A.-T. was supported by a grant from Sidaction (https://www.sidaction.org/)., ANR-10-LABX-0069,MILIEU INTERIEUR,GENETIC & ENVIRONMENTAL CONTROL OF IMMUNE PHENOTYPE VARIANCE: ESTABLISHING A PATH TOWARDS PERSONALIZED MEDICINE(2010), Agence Nationale de Recherches sur le sida et les hépatites virales (Francia), Institut National de la Santé et de la Recherche Médicale (Francia), Institut Pasteur, Paul Sabatier University (Francia), Milieu Intérieur Program, Instituto de Salud Carlos III, Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Pathogénie Virale - Viral Pathogenesis, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Génomes, biologie cellulaire et thérapeutiques (GenCellDi (U944 / UMR7212)), Collège de France (CdF (institution))-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), CHU Henri Mondor [Créteil], Service Maladies infectieuses et tropicales [CHU Toulouse], Pôle Inflammation, infection, immunologie et loco-moteur [CHU Toulouse] (Pôle I3LM Toulouse), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Laboratoire Virologie [CHU Toulouse], Institut Fédératif de Biologie (IFB), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Pôle Biologie [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Gestionnaire, Hal Sorbonne Université, Laboratoires d'excellence - GENETIC & ENVIRONMENTAL CONTROL OF IMMUNE PHENOTYPE VARIANCE: ESTABLISHING A PATH TOWARDS PERSONALIZED MEDICINE - - MILIEU INTERIEUR2010 - ANR-10-LABX-0069 - LABX - VALID, Agence Nationale de Recherches sur le SIDA et les Hépatites Virales (France), Institut National de la Santé et de la Recherche Médicale (France), and Université Paul Sabatier Toulouse III

Subjects
RNA viruses, CD4-Positive T-Lymphocytes, MESH: CD4-Positive T-Lymphocytes / virology, [SDV]Life Sciences [q-bio], HIV Infections, chemokines, Pathology and Laboratory Medicine, MESH: Viral Envelope Proteins / metabolism, MESH: Virulence Substances, White Blood Cells, Spectrum Analysis Techniques, cell staining, Immunodeficiency Viruses, Viral Envelope Proteins, Animal Cells, Medicine and Health Sciences, Homeostasis, viral tropism, MESH: HIV Infections / physiopathology, Biology (General), Virulence, T Cells, Chemotaxis, MESH: Antiviral Agents / metabolism, Flow Cytometry, MESH: Chemokine CXCL12 / metabolism, [SDV] Life Sciences [q-bio], Cell Motility, Medical Microbiology, Spectrophotometry, MESH: Homeostasis, Viruses, Cytophotometry, Pathogens, Cellular Types, Research Article, Cell Physiology, Receptors, CXCR4, QH301-705.5, Immune Cells, Immunology, cloning, MESH: HIV-1 / physiology, MESH: HIV-1 / pathogenicity, Research and Analysis Methods, Microbiology, Antiviral Agents, MESH: HIV Infections / transmission, MESH: Receptors, CXCR4 / metabolism, Retroviruses, Humans, MESH: HIV Infections / virology, Molecular Biology Techniques, cell binding, Microbial Pathogens, Molecular Biology, Blood Cells, cell fusion, MESH: Humans, Lentivirus, Organisms, Biology and Life Sciences, HIV, Cell Biology, RC581-607, Chemokine CXCL12, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, HIV-1, viral pathogens, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Immunologic diseases. Allergy
Abstract

HIV-1 infects CD4 T lymphocytes (CD4TL) through binding the chemokine receptors CCR5 or CXCR4. CXCR4-using viruses are considered more pathogenic, linked to accelerated depletion of CD4TL and progression to AIDS. However, counterexamples to this paradigm are common, suggesting heterogeneity in the virulence of CXCR4-using viruses. Here, we investigated the role of the CXCR4 chemokine CXCL12 as a driving force behind virus virulence. In vitro, CXCL12 prevents HIV-1 from binding CXCR4 and entering CD4TL, but its role in HIV-1 transmission and propagation remains speculative. Through analysis of thirty envelope glycoproteins (Envs) from patients at different stages of infection, mostly treatment-naïve, we first interrogated whether sensitivity of viruses to inhibition by CXCL12 varies over time in infection. Results show that Envs resistant (RES) to CXCL12 are frequent in patients experiencing low CD4TL levels, most often late in infection, only rarely at the time of primary infection. Sensitivity assays to soluble CD4 or broadly neutralizing antibodies further showed that RES Envs adopt a more closed conformation with distinct antigenicity, compared to CXCL12-sensitive (SENS) Envs. At the level of the host cell, our results suggest that resistance is not due to improved fusion or binding to CD4, but owes to viruses using particular CXCR4 molecules weakly accessible to CXCL12. We finally asked whether the low CD4TL levels in patients are related to increased pathogenicity of RES viruses. Resistance actually provides viruses with an enhanced capacity to enter naive CD4TL when surrounded by CXCL12, which mirrors their situation in lymphoid organs, and to deplete bystander activated effector memory cells. Therefore, RES viruses seem more likely to deregulate CD4TL homeostasis. This work improves our understanding of the pathophysiology and the transmission of HIV-1 and suggests that RES viruses’ receptors could represent new therapeutic targets to help prevent CD4TL depletion in HIV+ patients on cART., Author summary HIV-1 infects immune cells by binding CD4 and a coreceptor, CCR5 or CXCR4. CXCR4-using viruses are thought to accelerate depletion of CD4 T lymphocytes (CD4TL) and AIDS development. This paradigm, while often true, is however not seen in all patients, suggesting heterogeneity in the virulence of viruses. Here, we show that CXCR4-using viruses can be discriminated on the basis of their resistance to the anti-HIV-1 effect of the CXCR4 chemokine CXCL12. Resistant (RES) viruses are found in patients with low CD4TL levels. They are featured by unique properties of their envelope glycoprotein and the way they use CXCR4. Our data also indicate that RES viruses could contribute to CD4TL depletion. They more effectively kill bystander activated effector memory CD4TL, a subset of CD4TL enriched in HIV+ patients, and enter CD4TL subsets surrounded by CXCL12. Resistance could therefore enhance the ability of viruses to target naive cells and their precursors in lymphoid organs where CXCL12 is present, further hindering CD4TL renewal. Beyond presenting a novel view of CXCR4-using HIV-1 pathogenesis, this work also opens new therapeutic perspectives and increases our knowledge of the still debated role of CXCL12 in HIV-1 transmission.

Published
2021

7. Productive HIV-1 infection of tissue macrophages by fusion with infected CD4+ T cells.

Author

Mascarau, Rémi, Woottum, Marie, Fromont, Léa, Gence, Rémi, Cantaloube-Ferrieu, Vincent, Vahlas, Zoï, Lévêque, Kevin, Bertrand, Florent, Beunon, Thomas, Métais, Arnaud, El Costa, Hicham, Jabrane-Ferrat, Nabila, Gallois, Yohan, Guibert, Nicolas, Davignon, Jean-Luc, Favre, Gilles, Maridonneau-Parini, Isabelle, Poincloux, Renaud, Lagane, Bernard, and Bénichou, Serge

Subjects
*T cells, *MACROPHAGES, *CELL fusion, *HIV, *TONSILS, *INFECTION, *ACTOMYOSIN
Abstract

Macrophages are essential for HIV-1 pathogenesis and represent major viral reservoirs. Therefore, it is critical to understand macrophage infection, especially in tissue macrophages, which are widely infected in vivo, but poorly permissive to cell-free infection. Although cell-to-cell transmission of HIV-1 is a determinant mode of macrophage infection in vivo, how HIV-1 transfers toward macrophages remains elusive. Here, we demonstrate that fusion of infected CD4+ T lymphocytes with human macrophages leads to their efficient and productive infection. Importantly, several tissue macrophage populations undergo this heterotypic cell fusion, including synovial, placental, lung alveolar, and tonsil macrophages. We also find that this mode of infection is modulated by the macrophage polarization state. This fusion process engages a specific short-lived adhesion structure and is controlled by the CD81 tetraspanin, which activates RhoA/ROCK-dependent actomyosin contractility in macrophages. Our study provides important insights into the mechanisms underlying infection of tissue-resident macrophages, and establishment of persistent cellular reservoirs in patients. [ABSTRACT FROM AUTHOR]

Published
2023
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8. Mechanisms of HIV-1 evasion to the antiviral activity of chemokine CXCL12 indicate potential links with pathogenesis.

Author

Armani-Tourret M, Zhou Z, Gasser R, Staropoli I, Cantaloube-Ferrieu V, Benureau Y, Garcia-Perez J, Pérez-Olmeda M, Lorin V, Puissant-Lubrano B, Assoumou L, Delaugerre C, Lelièvre JD, Lévy Y, Mouquet H, Martin-Blondel G, Alcami J, Arenzana-Seisdedos F, Izopet J, Colin P, and Lagane B

Subjects
CD4-Positive T-Lymphocytes virology, HIV Infections physiopathology, HIV Infections transmission, HIV-1 physiology, Homeostasis, Humans, Viral Envelope Proteins metabolism, Virulence, Antiviral Agents metabolism, Chemokine CXCL12 metabolism, HIV Infections virology, HIV-1 pathogenicity, Receptors, CXCR4 metabolism
Abstract

HIV-1 infects CD4 T lymphocytes (CD4TL) through binding the chemokine receptors CCR5 or CXCR4. CXCR4-using viruses are considered more pathogenic, linked to accelerated depletion of CD4TL and progression to AIDS. However, counterexamples to this paradigm are common, suggesting heterogeneity in the virulence of CXCR4-using viruses. Here, we investigated the role of the CXCR4 chemokine CXCL12 as a driving force behind virus virulence. In vitro, CXCL12 prevents HIV-1 from binding CXCR4 and entering CD4TL, but its role in HIV-1 transmission and propagation remains speculative. Through analysis of thirty envelope glycoproteins (Envs) from patients at different stages of infection, mostly treatment-naïve, we first interrogated whether sensitivity of viruses to inhibition by CXCL12 varies over time in infection. Results show that Envs resistant (RES) to CXCL12 are frequent in patients experiencing low CD4TL levels, most often late in infection, only rarely at the time of primary infection. Sensitivity assays to soluble CD4 or broadly neutralizing antibodies further showed that RES Envs adopt a more closed conformation with distinct antigenicity, compared to CXCL12-sensitive (SENS) Envs. At the level of the host cell, our results suggest that resistance is not due to improved fusion or binding to CD4, but owes to viruses using particular CXCR4 molecules weakly accessible to CXCL12. We finally asked whether the low CD4TL levels in patients are related to increased pathogenicity of RES viruses. Resistance actually provides viruses with an enhanced capacity to enter naive CD4TL when surrounded by CXCL12, which mirrors their situation in lymphoid organs, and to deplete bystander activated effector memory cells. Therefore, RES viruses seem more likely to deregulate CD4TL homeostasis. This work improves our understanding of the pathophysiology and the transmission of HIV-1 and suggests that RES viruses' receptors could represent new therapeutic targets to help prevent CD4TL depletion in HIV+ patients on cART., Competing Interests: The authors have declared that no competing interests exist.

Published
2021
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