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The heat shock protein Hsc70-3 mediates an anti-apoptotic response critical for Plasmodium evasion of Anopheles gambiae immunity.

Thiago Luiz Alves E SilvaGaspar E CanepaBrendan SweeneyPatricia Hessab AlvarengaMing ZhaoJoel Vega-RodríguezAlvaro Molina-CruzCarolina Barillas-Mury
Published in: Microbiology spectrum (2023)
mosquitoes is very effective, in part because the parasite expresses a surface protein called Pfs47 that allows it to evade the mosquito immune system. Here we investigate how this protein changes the response of mosquito midgut epithelial cells to invasion by the parasite. Pfs47 is known to interact with P47Rec, a mosquito midgut receptor. We found that Pf47Rec inhibits caspase-mediated apoptosis by interacting with the Hsc70-3. This disrupts nitration of midgut epithelial cells invaded by the parasite and the release of hemocyte-derived microvesicles, which are critical for effective activation of the mosquito complement system that eliminates the parasite.
Keyphrases
  • aedes aegypti
  • plasmodium falciparum
  • zika virus
  • heat shock protein
  • dengue virus
  • toxoplasma gondii
  • trypanosoma cruzi
  • cell death
  • life cycle
  • amino acid
  • oxidative stress
  • induced apoptosis
  • protein kinase