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- W1923112544 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." @default.
- W1923112544 created "2016-06-24" @default.
- W1923112544 creator A5016090427 @default.
- W1923112544 creator A5051420141 @default.
- W1923112544 creator A5067893149 @default.
- W1923112544 creator A5070908421 @default.
- W1923112544 date "2015-07-29" @default.
- W1923112544 modified "2023-10-18" @default.
- W1923112544 title "The influence of host genetics on erythrocytes and malaria infection: is there therapeutic potential?" @default.
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