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Cell Host Microbe. 2017 Aug 9;22(2):232-245. doi: 10.1016/j.chom.2017.07.003.

The Molecular Basis of Erythrocyte Invasion by Malaria Parasites.

Author information

1
The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, VIC 3052, Australia; Department of Medical Biology, University of Melbourne, Parkville, VIC 3010, Australia. Electronic address: cowman@wehi.edu.au.
2
The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, VIC 3052, Australia; Department of Medical Biology, University of Melbourne, Parkville, VIC 3010, Australia.
3
Harvard T. H. Chan School of Public Health, Harvard University, Cambridge, MA, USA.

Abstract

Plasmodium species cause malaria by proliferating in human erythrocytes. Invasion of immunologically privileged erythrocytes provides a relatively protective niche as well as access to a rich source of nutrients. Plasmodium spp. target erythrocytes of different ages, but share a common mechanism of invasion. Specific engagement of erythrocyte receptors defines target cell tropism, activating downstream events and resulting in the physical penetration of the erythrocyte, powered by the parasite's actinomyosin-based motor. Here we review the latest in our understanding of the molecular composition of this highly complex and fascinating biological process.

KEYWORDS:

Plasmodium; erythrocyte; falciparum; invasion; malaria; merozoite; vivax

PMID:
28799908
DOI:
10.1016/j.chom.2017.07.003
[Indexed for MEDLINE]
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