title: Plasmodium falciparum is able to invade erythrocytes through a trypsin-resistant pathway independent of glycophorin B.
abstract: Plasmodium falciparum invades erythrocytes through multiple ligand-receptor interactions, with redundancies in each pathway. One such alternate pathway is the trypsin-resistant pathway that enables P. falciparum to invade trypsin-treated erythrocytes. Previous studies have shown that this trypsin-resistant pathway is dependent on glycophorin B, as P. falciparum strains invade trypsin-digested glycophorin B-deficient erythrocytes at a highly reduced efficiency. Furthermore, in a recent study, the P. falciparum 7G8 strain did not invade glycophorin B-deficient erythrocytes, a finding that was not confirmed in the present study. To analyze the degree of dependence on glycophorin B for invasion by P. falciparum through the trypsin-resistant pathway, we have studied the invasion phenotypes of five parasite strains, 3D7, HB3, Dd2, 7G8, and Indochina I, on trypsin-treated normal and glycophorin B-deficient erythrocytes. Invasion was variably reduced in glycophorin B-deficient erythrocytes. Four strains, 3D7, HB3, Dd2, and Indochina I, invaded trypsin-treated erythrocytes, while invasion by the 7G8 strain was reduced by 90%. Among the four strains, invasion by 3D7, HB3, and Dd2 of trypsin-digested glycophorin B-deficient erythrocytes was further reduced. However, Indochina I invaded trypsin-digested glycophorin B-deficient erythrocytes at the same efficiency as its invasion of trypsin-digested normal erythrocytes. This strongly suggests that the Indochina I strain of P. falciparum is not dependent on glycophorin B to invade through a trypsin-resistant pathway as are the strains 3D7, HB3, and Dd2. Thus, P. falciparum is able to invade erythrocytes through a glycophorin B-independent, trypsin-resistant pathway.
authors.affiliation: Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
authors.forename: Deepak
authors.initials: D
authors.lastname: Gaur
authors.forename: Jill R
authors.initials: JR
authors.lastname: Storry
authors.forename: Marion E
authors.initials: ME
authors.lastname: Reid
authors.forename: John W
authors.initials: JW
authors.lastname: Barnwell
authors.forename: Louis H
authors.initials: LH
authors.lastname: Miller
mesh_terms: D000818:Animals; D004351:Drug Resistance; D004912:Erythrocytes / Q000378:metabolism / Q000469:parasitology*; D006021:Glycophorins / Q000378:metabolism*; D006801:Humans; D016778:Malaria, Falciparum / Q000469:parasitology; D010963:Plasmodium falciparum / Q000472:pathogenicity*; D014357:Trypsin / Q000378:metabolism / Q000494:pharmacology
chemical_list: D006021:Glycophorins; D014357:Trypsin