Journal article

Interactions of human microglia cells with Japanese encephalitis virus

  • Lannes, Nils Department of Medicine, Unit of Anatomy, University of Fribourg, Switzerland
  • Neuhaus, Viviane Department of Medicine, Unit of Anatomy, University of Fribourg, Switzerland
  • Scolari, Brigitte Department of Medicine, Unit of Anatomy, University of Fribourg, Switzerland
  • Kharoubi-Hess, Solange Department of Medicine, Unit of Anatomy, University of Fribourg, Switzerland
  • Walch, Michael Department of Medicine, Unit of Anatomy, University of Fribourg, Switzerland
  • Summerfield, Artur Institute of Virology and Immunology, Mittelhäusern, Switzerland - Department of Infectious Diseases and Pathobiology, Vetsuisse Faculty, University of Bern, Switzerland.
  • Filgueira, Luis Department of Medicine, Unit of Anatomy, University of Fribourg, Switzerland
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    2017
Published in:
  • Virology Journal. - 2017, vol. 14, p. 8
English Japanese encephalitis virus (JEV) is a neurotropic flavivirus causing mortality and morbidity in humans. Severe Japanese encephalitis cases display strong inflammatory responses in the central nervous system and an accumulation of viral particles in specific brain regions. Microglia cells are the unique brain-resident immune cell population with potent migratory functions and have been proposed to act as a viral reservoir for JEV. Animal models suggest that the targeting of microglia by JEV is partially responsible for inflammatory reactions in the brain. Nevertheless, the interactions between human microglia and JEV are poorly documented.Methods: Using human primary microglia and a new model of human blood monocyte-derived microglia, the present study explores the interaction between human microglia and JEV as well as the role of these cells in viral transmission to susceptible cells. To achieve this work, vaccine-containing inactivated JEV and two live JEV strains were applied on human microglia.Results: Live JEV was non-cytopathogenic to human microglia but increased levels of CCL2, CXCL9 and CXCL10 in such cultures. Furthermore, human microglia up-regulated the expression of the fraktalkine receptor CX3CR1 upon exposure to both JEV vaccine and live JEV. Although JEV vaccine enhanced MHC class II on all microglia, live JEV enhanced MHC class II mainly on CX3CR1+ microglia cells. Importantly, human microglia supported JEV replication, but infectivity was only transmitted to neighbouring cells in a contact-dependent manner.Conclusion: Our findings suggest that human microglia may be a source of neuronal infection and sustain JEV brain pathogenesis.
Faculty
Faculté des sciences et de médecine
Department
Département de Médecine
Language
  • English
Classification
Biology
License
License undefined
Identifiers
Persistent URL
https://folia.unifr.ch/unifr/documents/305268
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