@article{fdi:010069322,
  title = {{A}xl mediates {ZIKA} virus entry in human glial cells and modulates innate immune responses},
  author = {{M}eertens, {L}. and {L}abeau, {A}. and {D}ejarnac, {O}. and {C}ipriani, {S}. and {S}inigaglia, {L}. and {B}onnet-{M}adin, {L}. and {L}e {C}harpentier, {T}. and {H}afirassou, {M}. {L}. and {Z}amborlini, {A}. and {C}ao-{L}ormeau, {V}. {M}. and {C}oulpier, {M}. and {M}iss{\'e}, {D}oroth{\'e}e and {J}ouvenet, {N}. and {T}abibiazar, {R}. and {G}ressens, {P}. and {S}chwartz, {O}. and {A}mara, {A}.},
  editor = {},
  language = {{ENG}},
  abstract = {{ZIKA} virus ({ZIKV}) is an emerging pathogen responsible for neurological disorders and congenital microcephaly. {H}owever, the molecular basis for {ZIKV} neurotropism remains poorly understood. {H}ere, we show that {A}xl is expressed in human microglia and astrocytes in the developing brain and that itmediates {ZIKV} infection of glial cells. {A}xl-mediated {ZIKV} entry requires the {A}xl ligand {G}as6, which bridges {ZIKV} particles to glial cells. {F}ollowing binding, {ZIKV} is internalized through clathrin-mediated endocytosis and traffics to {R}ab5+ endosomes to establish productive infection. {D}uring entry, the {ZIKV}/{G}as6 complex activates {A}xl kinase activity, which downmodulates interferon signaling and facilitates infection. {ZIKV} infection of human glial cells is inhibited by {MYD}1, an engineered {A}xl decoy receptor, and by the {A}xl kinase inhibitor {R}428. {O}ur results highlight the dual role of {A}xl during {ZIKV} infection of glial cells: promoting viral entry and modulating innate immune responses. {T}herefore, inhibiting {A}xl function may represent a potential target for future antiviral therapies.},
  keywords = {},
  booktitle = {},
  journal = {{C}ell {R}eports},
  volume = {18},
  numero = {2},
  pages = {324--333},
  ISSN = {2211-1247},
  year = {2017},
  DOI = {10.1016/j.celrep.2016.12.045},
  URL = {https://www.documentation.ird.fr/hor/fdi:010069322},
}