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Infection and Immunity, December 2003, p. 6742-6746, Vol. 71, No. 12
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.12.6742-6746.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Plasmodium falciparum Is Able To Invade Erythrocytes through a Trypsin-Resistant Pathway Independent of Glycophorin B

Deepak Gaur,1 Jill R. Storry,2 Marion E. Reid,2 John W. Barnwell,3 and Louis H. Miller1*

Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892,1 Immunohaematology Laboratory, New York Blood Center, New York, New York 10021,2 Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Chamblee, Georgia 303413

Received 17 June 2003/ Returned for modification 8 August 2003/ Accepted 3 September 2003

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.

* Corresponding author. Mailing address: Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 4 Center Dr., Building 4, Room B1-41, Bethesda, MD 20892. Phone: (301) 496-2183. Fax: (301) 402-2201. E-mail: lmiller{at}niaid.nih.gov.

Editor: W. A. Petri, Jr.

Infection and Immunity, December 2003, p. 6742-6746, Vol. 71, No. 12
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.12.6742-6746.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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  • Mayer, D. C. G., Cofie, J., Jiang, L., Hartl, D. L., Tracy, E., Kabat, J., Mendoza, L. H., Miller, L. H. (2009). Glycophorin B is the erythrocyte receptor of Plasmodium falciparum erythrocyte-binding ligand, EBL-1. Proc. Natl. Acad. Sci. USA 106: 5348-5352 [Abstract] [Full Text]  
  • Kadekoppala, M., O'Donnell, R. A., Grainger, M., Crabb, B. S., Holder, A. A. (2008). Deletion of the Plasmodium falciparum Merozoite Surface Protein 7 Gene Impairs Parasite Invasion of Erythrocytes. Eukaryot Cell 7: 2123-2132 [Abstract] [Full Text]  
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