Article

Hemoglobins S and C Interfere with Actin Remodeling in Plasmodium falciparum–Infected Erythrocytes

Department of Infectious Diseases, Parasitology, Heidelberg University, 69120 Heidelberg, Germany.
Science (impact factor: 31.2). 12/2011; 334(6060):1283-1286. DOI:10.1126/science.1213775 pp.1283-1286

ABSTRACT The hemoglobins S and C protect carriers from severe Plasmodium falciparum malaria. Here, we found that these hemoglobinopathies affected the trafficking system that directs parasite-encoded proteins
to the surface of infected erythrocytes. Cryoelectron tomography revealed that the parasite generated a host-derived actin
cytoskeleton within the cytoplasm of wild-type red blood cells that connected the Maurer’s clefts with the host cell membrane
and to which transport vesicles were attached. The actin cytoskeleton and the Maurer’s clefts were aberrant in erythrocytes
containing hemoglobin S or C. Hemoglobin oxidation products, enriched in hemoglobin S and C erythrocytes, inhibited actin
polymerization in vitro and may account for the protective role in malaria.

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Keywords

C. Hemoglobin oxidation products
 
directs parasite-encoded proteins
 
hemoglobinopathies
 
hemoglobins S
 
host cell membrane
 
protective role
 
severe Plasmodium falciparum malaria
 
trafficking system
 
transport vesicles
 
wild-type red blood cells