<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Lannes, Nils</dc:creator>
  <dc:creator>Neuhaus, Viviane</dc:creator>
  <dc:creator>Scolari, Brigitte</dc:creator>
  <dc:creator>Kharoubi-Hess, Solange</dc:creator>
  <dc:creator>Walch, Michael</dc:creator>
  <dc:creator>Summerfield, Artur</dc:creator>
  <dc:creator>Filgueira, Luis</dc:creator>
  <dc:date>2017</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">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.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/305268</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/305268/files/fil_ihm.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1186/s12985-016-0675-3</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>Virology Journal. - 2017, vol. 14, p. 8</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Human microglia</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Japanese encephalitis virus</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Inflammation</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Chemokine ligand-receptor</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Viral transmission</dc:subject>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns6="xml" ns6:lang="en">Interactions of human microglia cells with Japanese encephalitis virus</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>