Sickle-cell disease (SCD) is a genetic
blood disorder in red blood cells. The disease is autosomal recessive, and it
turns the erythrocytes into a sickle shape instead of the normal rod-shaped.
The new shape is caused by a mutation in a hemoglobin gene. People with SCD can
have a variety of complications ranging from anemia to a stroke. The
interesting part about sickle-cell disease is its prevalence in sub-tropical
sub-Saharan regions. These regions are also known to have high cases of
malaria, which is a disease caused by protists of the genus Plasmodium. People
with the autosomal recessive disease, or people who carry the sickle cell
trait, are known to be resistant to the Plasmodium
falciparum. Therefore, natural selection takes place in these areas with
high cases of malaria, and the sickle cell trait gets passed on.
Researchers have studied the role of
the sickle cell hemoglobin (HbS) in sub-Saharan Africa where “moderate-to-intense
malaria transmission” is present (Terlouw). A lot of the children there tended
to have the sickle cell trait, which is why researchers decided to study the
effect of a particular antimalarial drug on young children. More specifically,
they were trying to determine the effect of sulfadoxine-pyrimethamine to clear
P. falciparum parasites. They found that those children with the sickle cell
trait reacted to the drug a lot better than those without the trait (Terlouw).
Natural selection acts again. The sickle cell trait outcompeted the dominant
trait when trying to survive in the presence of the drug. This cannot be due to
random selection because the sickle cell trait remained in high quantity among
the children, which further demonstrated that natural selection took place. If
we continue to make drugs to cure diseases, it is important that we take
evolution into account because it will give us a better understanding of how to
fight off these different diseases such as malaria.
Word Count: 313
Source
Feiko O. ter Kuile, et al.
"Increased Efficacy Of Sulfadoxine-Pyrimethamine In The Treatment Of
Uncomplicated Falciparum Malaria Among Children With Sickle Cell Trait In
Western Kenya." The Journal Of Infectious Diseases 11 (2002): 1661.
JSTOR Life Sciences. Web. 18 Feb. 2013.
Alyssa Thomas
The children with the sickle cell allele reacted to the antimalarial drug "a lot better"...so what does this mean for the children with the allele for normal shaped blood cells? selection implies differential survival, but I hope this doesn't mean that the children without the sickle cell allele succumbed to the antimalarial drug at a higher rate...in which case, it's not a very good drug and should be re-evaluated
ReplyDeleteCan you define "a lot better" in regards to how the children with a sickle cell trait react to the medication? It would be nice to see how well they responded and how this response held its strength with time.
ReplyDelete-Mary Morales
Did the scientists have any theories as to why sickle cell trait kids responded better to the drugs? Additionally, how do they isolate efficacy of the drug from inherent resistance of sickle cell trait patients to malaria?
ReplyDelete-Tom Xia
I would not call this a natural selection. The presence of drug actually makes it an artificial selection. I am not even sure if the children with sickle cell will necessarily "outcompete the dominant" because they still suffer from sickle cell anemia. Also remember in class we discuss about how the presence of sickle cell could be due to the heterozygote advantage to malaria, which increases the number of gene carriers.
ReplyDeleteIsn't having the heterozygous sickle cell trait the most advantageous in that it fights malaria without them actually having the full sickle cell disease? How does the heterozygous rate compare to the sickle cell trait when it comes to malaria?
ReplyDeleteI am a bit confused as to the results of this drug treatment. If I understand correctly, the drug treatment showed better efficacy in those children who carried the sickle cell trait (heterozygous) than those who did not have the trait or disease at all (homogeneous dominant). Though, the drug might have shown better results for those who were carriers, I don't believe that this really has to do with "out-competing" those who were homogeneous dominant. As stated previously stated by Peter and Briona, I would more attribute this phenomenon to heterozygous advantage. Additionally, if the frequency of the sickle cell trait still remained quite high after use of the drug, for how many generations was the drug tested? If it was to provide some sort of advantage for natural selection, then wouldn't the results of the drug have to be shown over many generations in humans?
ReplyDelete