The malaria parasite continues to plague humanity and the death toll is enormous. Much effort has been devoted to studying its life cycle and all identifiable natural mechanisms giving resistance. The best known trait conferring resistance is sickle cell anaemia: this affects red blood cells so that the malaria parasite (Plasmodium falciparum) does not gain a foothold in the body, but at the same time it adversely affects the functionality of the blood so that the human is regarded as having a genetic disease.

Mosquitoes can transmit malaria
It has been found recently that red blood cells from patients with pyruvate kinase deficiency are resistant to invasion by the malaria parasite. Furthermore, those cells that do succumb to infection are more rapidly cleared by macrophages than are infected cells from control subjects. Kevin Kain, one of the lead researchers on the project is quoted as saying: "Our research shows that people who have an enzyme deficiency or those who carry the gene trait for this deficiency may be protected from severe and fatal malaria." It is hoped that the findings will lead to the design of novel therapies by enhancing the body's protective pathways instead of inundating the body with drugs.
This research brings to mind Michael Behe's analysis of malaria research findings for understanding what Darwinian mechanisms can and cannot do. To explain his conclusions, he rejected the analogy of an arms race (often used by Darwinians to describe the outcome of the struggle for survival). In the struggle against the malaria parasite, we do not see an arms race (with the incremental refinement of weapons). Rather, according to Behe, we see trench warfare. In wartime, a bridge could be blown up to prevent the enemy from crossing; a tree could be felled across a railway track to create disruption. The trench warfare analogy fits malaria well (sickle cell anaemia involves damage to the red blood cells, and in this case, resistance is conferred by pyruvate kinase deficiency). The same lessons are learned from antibiotic resistance, which might arise as a loss of a transporter or the alteration of a ribosome.
Darwinians say that we can obtain new functions by mutation and selection, but the evidence is that loss of function is the explanation for both resistance against malaria and antibiotic resistance.
Pyruvate Kinase Deficiency and Malaria
Kodjo Ayi, Gundula Min-Oo, Lena Serghides, Maryanne Crockett, Melanie Kirby-Allen, Ian Quirt, Philippe Gros, and Kevin C. Kain.
The New England Journal of Medicine, 358(17), April 24 2008, 1805-1810.
SUMMARY: Malaria that is caused by Plasmodium falciparum is a significant global health problem. Genetic characteristics of the host influence the severity of disease and the ultimate outcome of infection, and there is evidence of coevolution of the plasmodium parasite with its host. In humans, pyruvate kinase deficiency is the second most common erythrocyte enzyme disorder. Here, we show that pyruvate kinase deficiency provides protection against infection and replication of P. falciparum in human erythrocytes, raising the possibility that mutant pyruvate kinase alleles may confer a protective advantage against malaria in human populations in areas where the disease is endemic.
See also:
Mutation In Human Gene Helps Protect Against Fatal Malaria, ScienceDaily (Apr. 22, 2008)
Behe, M. Malaria and Mutations, Mike Behe's Amazon Blog, May 9, 2008.
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