@article{fdi:010077462,
  title = {{I}ncreased mosquito midgut infection by dengue virus recruitment of plasmin is blocked by an endogenous {K}azal-type inhibitor},
  author = {{R}amesh, {K}. and {W}alvekar, {V}. {A}. and {W}ong, {B}. and {S}ayed, {A}. {M}. {M}. and {M}iss{\'e}, {D}oroth{\'e}e and {K}ini, {R}. {M}. and {M}ok, {Y}. {K}. and {P}ompon, {J}ulien},
  editor = {},
  language = {{ENG}},
  abstract = {{D}engue symptoms include alteration of blood coagulation and fibrinolysis, causing severe hemorrhage and death. {H}ere, we demonstrate that higher concentration of plasmin, the human fibrinolytic factor, in blood meal enhances dengue virus ({DENV}) infection in mosquito midgut and dissemination in mosquitoes. {W}e also show that mosquitoes express a plasmin-selective {K}azal-type inhibitor ({A}a{TI}) in the midgut to inhibit plasmin proteolysis and revert the enhanced infection. {U}sing bio-layer interferometry, we show that {DENV}, plasmin, and {A}a{TI} interact to form a tripartite complex. {E}ventually, plasmin increases midgut internalization of dextran molecules and this is reverted by {A}a{TI}. {O}ur study demonstrates that (1) {DENV} recruits plasmin to increase local proteolytic activity in the midgut, thus degrading the glycocalyx and enhancing {DENV} internalization and (2) {A}a{TI} can act as a transmission-blocking agent by inhibiting plasmin proteolysis. {O}ur results indicate that dengue pathogenesis enhances {DENV} fitness by increasing its infectivity to mosquitoes.},
  keywords = {},
  booktitle = {},
  journal = {{I}science},
  volume = {21},
  numero = {},
  pages = {564--+},
  year = {2019},
  DOI = {10.1016/j.isci.2019.10.056},
  URL = {https://www.documentation.ird.fr/hor/fdi:010077462},
}