@article{fdi:010074361,
  title = {{Z}ika virus infection modulates the metabolomic profile of microglial cells},
  author = {{D}iop, {F}od{\'e} and {V}ial, {T}homas and {F}erraris, {P}auline and {W}ichit, {S}. and {B}engue, {M}. and {H}amel, {R}odolphe and {T}alignani, {L}. and {L}i{\'e}geois, {F}lorian and {P}ompon, {J}ulien and {Y}ssel, {H}. and {M}arti, {G}. and {M}iss{\'e}, {D}oroth{\'e}e},
  editor = {},
  language = {{ENG}},
  abstract = {{Z}ika virus ({ZIKV}) is an emerging arbovirus of the {F}laviviridae family. {A}lthough infection with {ZIKV} generally leads to mild disease, its recent emergence in the {A}mericas has been associated with an increase in the development of the {G}uillain-{B}arre syndrome in adults, as well as with neurological complications, in particular congenital microcephaly, in new-borns. {T}o date, little information is available on neuroinflammation induced by {ZIKV}, notably in microglial cells in the context of their metabolic activity, a series of chemical transformations that are essential for their growth, reproduction, structural maintenance and environmental responses. {T}herefore, in the present study we investigated the metabolomic profile of {ZIKV}-infected microglia. {M}icroglial cells were exposed to {ZIKV} at different time points and were analyzed by a {L}iquid {C}hromatography-{H}igh {R}esolution mass spectrometry-based metabolomic approach. {T}he results show that {ZIKV} infection in microglia leads to modulation of the expression of numerous metabolites, including lysophospholipids, particulary {L}ysophosphatidylcholine, and phospholipids such as {P}hosphatidylcholine, {P}hosphatidylserine, {C}eramide and {S}phingomyelin, and carboxylicic acids as {U}ndecanedioic and {D}odecanedioic acid. {S}ome of these metabolites are involved in neuronal differentiation, regulation of apoptosis, virion architecture and viral replication. {ZIKV} infection was associated with concomitant secretion of inflammatory mediators linked with central nervous system inflammation such as {IL}-6, {TNF}-alpha, {IL}-beta, i{NOS} and {NO}. {I}t also resulted in the upregulation of the expression of the gene encoding {CX}3{CR}1, a chemokine receptor known to regulate functional synapse plasticity and signaling between microglial cells. {T}hese findings highlight an important role for microglia and their metabolites in the process of neuroinflammation that occurs during {ZIKV} pathogenesis.},
  keywords = {},
  booktitle = {},
  journal = {{PL}o{S} {O}ne},
  volume = {13},
  numero = {10},
  pages = {e0206093 [16 p.]},
  ISSN = {1932-6203},
  year = {2018},
  DOI = {10.1371/journal.pone.0206093},
  URL = {https://www.documentation.ird.fr/hor/fdi:010074361},
}