A role for apical membrane antigen 1 during invasion of hepatocytes by Plasmodium falciparum sporozoites.
Silvie, Olivier;
Franetich, Jean-François;
Charrin, Stéphanie;
Mueller, Markus S;
Siau, Anthony;
Bodescot, Myriam;
Rubinstein, Eric;
Hannoun, Laurent;
Charoenvit, Yupin;
Kocken, Clemens H;
+7 more...Thomas, Alan W;
Van Gemert, Geert-Jan;
Sauerwein, Robert W;
Blackman, Michael J;
Anders, Robin F;
Pluschke, Gerd;
Mazier, Dominique;
(2004)
A role for apical membrane antigen 1 during invasion of hepatocytes by Plasmodium falciparum sporozoites.
The Journal of biological chemistry, 279 (10).
pp. 9490-9496.
ISSN 0021-9258
DOI: https://doi.org/10.1074/jbc.M311331200
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Plasmodium sporozoites are transmitted through the bite of infected mosquitoes and invade hepatocytes as a first and obligatory step of the parasite life cycle in man. Hepatocyte invasion involves proteins secreted from parasite vesicles called micronemes, the most characterized being the thrombospondin-related adhesive protein (TRAP). Here we investigated the expression and function of another microneme protein recently identified in Plasmodium falciparum sporozoites, apical membrane antigen 1 (AMA-1). P. falciparum AMA-1 is expressed in sporozoites and is lost after invasion of hepatocytes, and anti-AMA-1 antibodies inhibit sporozoite invasion, suggesting that the protein is involved during invasion of hepatocytes. As observed with TRAP, AMA-1 is initially mostly sequestered within the sporozoite. Upon microneme exocytosis, AMA-1 and TRAP relocate to the sporozoite surface, where they are proteolytically cleaved, resulting in the shedding of soluble fragments. A subset of serine protease inhibitors blocks the processing and shedding of both AMA-1 and TRAP and inhibits sporozoite infectivity, suggesting that interfering with sporozoite proteolytic processing may constitute a valuable strategy to prevent hepatocyte infection.