Carriers of contracting the disease. Low levels

Carriers
of the sickle cell hemoglobin (SCH) gene are protected to a certain degree
against malaria. The researchers identified and tested the mechanism by which
this protection occurs and see it as a future target for treatment of this
disease.

Using
genetically modified mice containing one faulty copy of the sickle cell
hemoglobin gene, the researchers found that these mice were better protected
against malaria—the disease caused by the Plasmodium
parasite. It was previously thought that the SCH gene protected against the
infection of the Plasmodium parasite
itself. However, the actual protection mechanism works by preventing the
disease after the animal has already been infected.

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High
levels of the prosthetic group heme were present in free form in the blood of
the heterozygote mice, but largely missing from the blood of the normal mice. This
prosthetic group helps protect mice against malaria before infection from the
parasite. Nonetheless, high levels of heme in the blood after infection with the
Plasmodium parasite seemed to
increase the probability of contracting the disease. Low levels of free
circulating heme prompt the production of the enzyme heme oxygenase-1—HO-1—which
in turn releases carbon monoxide, a gas that is very toxic in large concentrations.
When found in low concentrations in the blood of the mice, carbon monoxide
actually seemed to help prevent accumulation of heme after the infection with the
Plasmodium parasite. The free heme in
the blood can therefore be both protective against malaria and dangerous at
once.

I
will use these results to demonstrate that the SCH gene provides a survival
advantage against malaria, which is a major reason why evolution has not
eliminated this gene completely, even though sickle cell anemia it is a disease
itself. Similarly, I will use this information to demonstrate that the HO-1
system, induced by the SCH gene, might be used therapeutically to treat severe
forms of malaria in the near future, presenting the possibility of potential treatment
for this parasitic disease. 327

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