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Malaria: modification of the red blood cell and consequences in the human host.

Moxon, Christopher A., Grau, George E. and Craig, Alister ORCID: https://orcid.org/0000-0003-0914-6164 (2011) 'Malaria: modification of the red blood cell and consequences in the human host.'. British Journal of Haematology, Vol 154, Issue 6, pp. 670-679.

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Abstract

Residence in the human erythrocyte is essential for the lifecycle of all Plasmodium that infect man. It is also the phase of the life cycle that causes disease. Although the red blood cell (RBC) is a highly specialized cell for its function of carrying oxygen to and carbon dioxide away from tissues, it is devoid of organelles and lacks any cellular machinery to synthesize new protein. Therefore in order to be able to survive and multiply within the RBC membrane the parasite needs to make many modifications to the infected RBC (iRBC). Plasmodium falciparum (P. falciparum) also expresses parasite-derived proteins on the surface of the iRBC that enable the parasite to cytoadhere to endothelial and other intravascular cells. These RBC modifications are at the root of malaria pathogenesis and, in this ancient disease of man, have formed the epicentre of a genetic 'battle' between parasite and host. This review discusses some of the critical modifications of the RBC by the parasite and some of the consequences of these adaptations on disease in the human host, with an emphasis on advances in understanding of the pathogenesis of severe and cerebral malaria (CM) from recent research.

Item Type: Article
Subjects: QX Parasitology > Protozoa > QX 135 Plasmodia
WC Communicable Diseases > Tropical and Parasitic Diseases > WC 755.1 General coverage
WH Hemic and Lymphatic Systems > Hematologic Diseases. Immunologic Factors. Blood Banks > WH 150 Erythrocytes
Digital Object Identifer (DOI): https://doi.org/10.1111/j.1365-2141.2011.08755.x
Depositing User: Mary Creegan
Date Deposited: 06 Sep 2011 08:18
Last Modified: 17 Jul 2019 14:14
URI: https://archive.lstmed.ac.uk/id/eprint/2029

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