The influence of host genetics on erythrocytes and malaria infection

is there therapeutic potential?

Patrick M. Lelliott*, Brendan J. McMorran, Simon J. Foote, Gaetan Burgio

*Corresponding author for this work

Research output: Contribution to journalReview article

21 Citations (Scopus)
4 Downloads (Pure)

Abstract

As parasites, Plasmodium species depend upon their host for survival. During the blood stage of their life-cycle parasites invade and reside within erythrocytes, commandeering host proteins and resources towards their own ends, and dramatically transforming the host cell. Parasites aptly avoid immune detection by minimizing the exposure of parasite proteins and removing themselves from circulation through cytoadherence. Erythrocytic disorders brought on by host genetic mutations can interfere with one or more of these processes, thereby providing a measure of protection against malaria to the host. This review summarizes recent findings regarding the mechanistic aspects of this protection, as mediated through the parasites interaction with abnormal erythrocytes. These novel findings include the reliance of the parasite on the host enzyme ferrochelatase, and the discovery of basigin and CD55 as obligate erythrocyte receptors for parasite invasion. The elucidation of these naturally occurring malaria resistance mechanisms is increasing the understanding of the host-parasite interaction, and as discussed below, is providing new insights into the development of therapies to prevent this disease.

Original languageEnglish
Article number289
Pages (from-to)1-15
Number of pages15
JournalMalaria Journal
Volume14
Issue number1
DOIs
Publication statusPublished - 29 Jul 2015
Externally publishedYes

Bibliographical note

Copyright the Author(s) 2015. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

Keywords

  • Cytoadherence
  • Erythrocyte
  • Growth
  • Host
  • Invasion
  • Malaria
  • Phagocytosis
  • Plasmodium
  • Polymorphism
  • Red blood cell

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