Talide L, Imler JL, Meignin C
Sensing Viral Infections in Insects: A Dearth of Pathway Receptors Article de journal
Dans: Curr Issues Mol Biol, vol. 34, p. 31-60, 2019, ISBN: 9781912530090.
Résumé | Liens | BibTeX | Étiquettes: imler, innate immunity, M3i, meignin, STAT, viral Infection
@article{Talide_2020,
title = {Sensing Viral Infections in Insects: A Dearth of Pathway Receptors},
author = {L Talide and JL Imler and C Meignin},
url = {https://www.caister.com/insectvirology2},
doi = {10.21775/cimb.034.031},
isbn = {9781912530090},
year = {2019},
date = {2019-06-06},
journal = {Curr Issues Mol Biol},
volume = {34},
pages = {31-60},
abstract = {Insects, the most diverse group of animals, can be infected by an extraordinary diversity of viruses. Among them, arthropod-borne viruses can be transmitted to humans, while bee and silkworm viruses cause important economic losses. Like all invertebrates, insects rely solely on innate immunity to counter viral infections. Protein-based mechanisms, involving restriction factors and evolutionarily conserved signaling pathways regulating transcription factors of the NF-kB and STAT families, participate in the control of viral infections in insects. In addition, RNA-based responses play a major role in the silencing of viral RNAs. We review here our current state of knowledge on insect antiviral defense mechanisms, which include conserved as well as adaptive, insect-specific strategies. Identification of the innate immunity receptors that sense viral infection in insects remains a major challenge for the field. },
keywords = {imler, innate immunity, M3i, meignin, STAT, viral Infection},
pubstate = {published},
tppubtype = {article}
}
Schaeffer Evelyne, Flacher Vincent, Neuberg Patrick, Hoste Astrid, Brulefert Adrien, Fauny Jean-Daniel, Wagner Alain, Mueller Christopher G
Inhibition of dengue virus infection by mannoside glycolipid conjugates Article de journal
Dans: Antiviral Research, vol. 154, p. 116–123, 2018, ISSN: 1872-9096.
Résumé | Liens | BibTeX | Étiquettes: Animals, Antiviral Agents, Cell Line, Cell Membrane, Chemistry, Chlorocebus aethiops, Dendritic Cells, Dengue, Dengue virus, development, Drug, Drug Discovery, Flavivirus, function, Fusion, Glycolipids, Health, Hep G2 Cells, Human, Humans, immunopathology, infection, inhibition, inhibitors, Inhibitory Concentration 50, lipid, Macrophages, Mannosides, Membrane, Serogroup, Skin, Team-Mueller, vaccine, Vaccines, Vero Cells, viral Infection, virus, Virus Replication
@article{schaeffer_inhibition_2018b,
title = {Inhibition of dengue virus infection by mannoside glycolipid conjugates},
author = {Evelyne Schaeffer and Vincent Flacher and Patrick Neuberg and Astrid Hoste and Adrien Brulefert and Jean-Daniel Fauny and Alain Wagner and Christopher G Mueller},
doi = {10.1016/j.antiviral.2018.04.005},
issn = {1872-9096},
year = {2018},
date = {2018-01-01},
journal = {Antiviral Research},
volume = {154},
pages = {116--123},
abstract = {Dengue virus (DENV), a mosquito-borne flavivirus, causes severe and potentially fatal symptoms in millions of infected individuals each year. Although dengue fever represents a major global public health problem, the vaccines or antiviral drugs proposed so far have not shown sufficient efficacy and safety, calling for new antiviral developments. Here we have shown that a mannoside glycolipid conjugate (MGC) bearing a trimannose head with a saturated lipid chain inhibited DENV productive infection. It showed remarkable cell promiscuity, being active in human skin dendritic cells, hepatoma cell lines and Vero cells, and was active against all four DENV serotypes, with an IC50 in the low micromolar range. Time-of-addition experiments and structure-activity analyses revealed the importance of the lipid chain to interfere with an early viral infection step. This, together with a correlation between antiviral activity and membrane polarization by the lipid moiety indicated that the inhibitor functions by blocking viral envelope fusion with the endosome membrane. These finding establish MGCs as a novel class of antivirals against the DENV.},
keywords = {Animals, Antiviral Agents, Cell Line, Cell Membrane, Chemistry, Chlorocebus aethiops, Dendritic Cells, Dengue, Dengue virus, development, Drug, Drug Discovery, Flavivirus, function, Fusion, Glycolipids, Health, Hep G2 Cells, Human, Humans, immunopathology, infection, inhibition, inhibitors, Inhibitory Concentration 50, lipid, Macrophages, Mannosides, Membrane, Serogroup, Skin, Team-Mueller, vaccine, Vaccines, Vero Cells, viral Infection, virus, Virus Replication},
pubstate = {published},
tppubtype = {article}
}
Schaeffer Evelyne, Flacher Vincent, Papageorgiou Vasiliki, Decossas Marion, Fauny Jean-Daniel, Krämer Melanie, Mueller Christopher G
Dermal CD14(+) Dendritic Cell and Macrophage Infection by Dengue Virus Is Stimulated by Interleukin-4 Article de journal
Dans: The Journal of Investigative Dermatology, vol. 135, no. 7, p. 1743–1751, 2015, ISSN: 1523-1747.
Résumé | Liens | BibTeX | Étiquettes: Abdominal Wall, Activation, Adhesion, adhesion molecules, Antigen-Presenting Cells, arbovirus, C-Type, Cell Adhesion, Cell Adhesion Molecules, Cell Surface, Cells, Chemistry, Confocal, Cultured, cytokine, Cytokines, cytology, Dendritic Cells, Dengue, Dengue virus, DERMAL DENDRITIC CELLS, Dermatitis, DERMIS, development, disease, Enzyme-Linked Immunosorbent Assay, Epidermal Cells, Epidermis, Human, Humans, ICAM-3, IL-4, Immunology, immunopathology, infection, Interleukin-4, Langerhans Cells, LECTIN, Lectins, Lymphocyte Activation, Macrophage, Macrophages, metabolism, Microscopy, pathogenicity, physiopathology, Receptor, Receptors, Scabies, Sensitivity and Specificity, Skin, Skin Diseases, SUBSETS, T CELL ACTIVATION, target, Team-Mueller, TNF ALPHA, Viral, viral Infection, Viral Load, virology, virus
@article{schaeffer_dermal_2015b,
title = {Dermal CD14(+) Dendritic Cell and Macrophage Infection by Dengue Virus Is Stimulated by Interleukin-4},
author = {Evelyne Schaeffer and Vincent Flacher and Vasiliki Papageorgiou and Marion Decossas and Jean-Daniel Fauny and Melanie Krämer and Christopher G Mueller},
doi = {10.1038/jid.2014.525},
issn = {1523-1747},
year = {2015},
date = {2015-07-01},
journal = {The Journal of Investigative Dermatology},
volume = {135},
number = {7},
pages = {1743--1751},
abstract = {Dengue virus (DENV) is responsible for the most prevalent arthropod-borne viral infection in humans. Events decisive for disease development occur in the skin after virus inoculation by the mosquito. Yet, the role of human dermis-resident immune cells in dengue infection and disease remains elusive. Here we investigated how dermal dendritic cells (dDCs) and macrophages (dMs) react to DENV and impact on immunopathology. We show that both CD1c(+) and CD14(+) dDC subsets were infected, but viral load greatly increased in CD14(+) dDCs upon IL-4 stimulation, which correlated with upregulation of virus-binding lectins Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Nonintegrin (DC-SIGN/CD209) and mannose receptor (CD206). IL-4 also enhanced T-cell activation by dDCs, which was further increased upon dengue infection. dMs purified from digested dermis were initially poorly infected but actively replicated the virus and produced TNF-α upon lectin upregulation in response to IL-4. DC-SIGN(+) cells are abundant in inflammatory skin with scabies infection or Th2-type dermatitis, suggesting that skin reactions to mosquito bites heighten the risk of infection and subsequent immunopathology. Our data identify dDCs and dMs as primary arbovirus target cells in humans and suggest that dDCs initiate a potent virus-directed T-cell response, whereas dMs fuel the inflammatory cascade characteristic of dengue fever.},
keywords = {Abdominal Wall, Activation, Adhesion, adhesion molecules, Antigen-Presenting Cells, arbovirus, C-Type, Cell Adhesion, Cell Adhesion Molecules, Cell Surface, Cells, Chemistry, Confocal, Cultured, cytokine, Cytokines, cytology, Dendritic Cells, Dengue, Dengue virus, DERMAL DENDRITIC CELLS, Dermatitis, DERMIS, development, disease, Enzyme-Linked Immunosorbent Assay, Epidermal Cells, Epidermis, Human, Humans, ICAM-3, IL-4, Immunology, immunopathology, infection, Interleukin-4, Langerhans Cells, LECTIN, Lectins, Lymphocyte Activation, Macrophage, Macrophages, metabolism, Microscopy, pathogenicity, physiopathology, Receptor, Receptors, Scabies, Sensitivity and Specificity, Skin, Skin Diseases, SUBSETS, T CELL ACTIVATION, target, Team-Mueller, TNF ALPHA, Viral, viral Infection, Viral Load, virology, virus},
pubstate = {published},
tppubtype = {article}
}
Kwan Wing-Hong, Helt Anna-Marija, Marañón Concepción, Barbaroux Jean-Baptiste, Hosmalin Anne, Harris Eva, Fridman Wolf H, Mueller Chris G F
Dendritic cell precursors are permissive to dengue virus and human immunodeficiency virus infection Article de journal
Dans: Journal of Virology, vol. 79, no. 12, p. 7291–7299, 2005, ISSN: 0022-538X.
Résumé | Liens | BibTeX | Étiquettes: ANTIGEN PRESENTING CELLS, Antigen-Presenting Cells, APC, BLOOD, CD8-Positive T-Lymphocytes, Cell Differentiation, Cells, COLONY-STIMULATING FACTOR, Cultured, Dendritic Cells, Dengue virus, Differentiation, Epidermis, Hematopoietic Stem Cells, HIV, HIV-1, Human, Humans, IMMATURE, immunodeficiency, infection, interleukin 10, Interleukin-10, Lipopolysaccharide Receptors, MEMORY T CELLS, monocyte, Monocytes, Necrosis, precursor, PROGENITORS, Skin, T CELLS, Team-Mueller, tumor, Tumor Necrosis Factor, viral Infection, virus
@article{kwan_dendritic_2005,
title = {Dendritic cell precursors are permissive to dengue virus and human immunodeficiency virus infection},
author = {Wing-Hong Kwan and Anna-Marija Helt and Concepción Marañón and Jean-Baptiste Barbaroux and Anne Hosmalin and Eva Harris and Wolf H Fridman and Chris G F Mueller},
doi = {10.1128/JVI.79.12.7291-7299.2005},
issn = {0022-538X},
year = {2005},
date = {2005-06-01},
journal = {Journal of Virology},
volume = {79},
number = {12},
pages = {7291--7299},
abstract = {CD14(+) interstitial cells reside beneath the epidermis of skin and mucosal tissue and may therefore play an important role in viral infections and the shaping of an antiviral immune response. However, in contrast to dendritic cells (DC) or blood monocytes, these antigen-presenting cells (APC) have not been well studied. We have previously described long-lived CD14(+) cells generated from CD34(+) hematopoietic progenitors, which may represent model cells for interstitial CD14(+) APC. Here, we show that these cells carry DC-SIGN and differentiate into immature DC in the presence of granulocyte-macrophage colony-stimulating factor. We have compared the CD14(+) cells and the DC derived from these cells with respect to dengue virus and human immunodeficiency virus type 1 (HIV-1) infection. Both cell types are permissive to dengue virus infection, but the CD14(+) cells secrete the anti-inflammatory cytokine interleukin 10 and no tumor necrosis factor alpha. Regarding HIV, the CD14(+) cells are permissive to HIV-1, release higher p24 levels than the derived DC, and more efficiently activate HIV Pol-specific CD8(+) memory T cells. The CD14(+) DC precursors infected with either virus retain their DC differentiation potential. The results suggest that interstitial CD14(+) APC may contribute to HIV-1 and dengue virus infection and the shaping of an antiviral immune response.},
keywords = {ANTIGEN PRESENTING CELLS, Antigen-Presenting Cells, APC, BLOOD, CD8-Positive T-Lymphocytes, Cell Differentiation, Cells, COLONY-STIMULATING FACTOR, Cultured, Dendritic Cells, Dengue virus, Differentiation, Epidermis, Hematopoietic Stem Cells, HIV, HIV-1, Human, Humans, IMMATURE, immunodeficiency, infection, interleukin 10, Interleukin-10, Lipopolysaccharide Receptors, MEMORY T CELLS, monocyte, Monocytes, Necrosis, precursor, PROGENITORS, Skin, T CELLS, Team-Mueller, tumor, Tumor Necrosis Factor, viral Infection, virus},
pubstate = {published},
tppubtype = {article}
}