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Infection and Immunity, January 2005, p. 649-651, Vol. 73, No. 1
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.1.649-651.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Molecular Parasitology, Lindsley Kimball Research Institute, New York Blood Center, New York, New York
Received 12 August 2004/ Returned for modification 16 September 2004/ Accepted 18 September 2004
Babesiosis has long been recognized as an economically important disease of cattle, but only in the last 30 years has Babesia been recognized as an important pathogen in humans. Invasion of erythrocytes is an integral part of the Babesia life cycle. However, very little information is available on the molecules involved in this process, in contrast to another hemoparasite, Plasmodium falciparum. Using invasion assays into normal red blood cells (RBCs), enzyme-treated cells, and clinically mutant cells, we showed that Babesia divergens uses neuraminidase- and trypsin-sensitive receptors to enter the RBCs, of which glycophorins A and B are the prominent ones. These results could have broad implications relating to evolutionarily conserved mechanisms of host cell entry in these related Apicomplexan parasites and pave the way toward a detailed molecular analysis of erythrocyte invasion in B. divergens.
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