It was recognized that thalassaemia was and still is particularly prevalent in areas in which malaria is or was endemic. The malaria parasite is an infectious agent carried by some types of mosquitoes, including mainly the anopheles type and enters the human body through a mosquito bite. The malaria parasite causes a serious infectious disease in humans by attacking the red blood cells. It is thought that in areas where malaria was endemic, humans underwent a small genetic change or adjustment in their DNA which gave them an advantage over those in whom this change did not occur, i.e. this change made them more resilient to the malaria infection. This is because important changes occurred in the environment of the red cells following this genetic change that did not allow the parasite to survive and multiply causing illness and death. This adjustment led to what we today know as the β-thalassaemia carrier status. As with the case of α- thalassaemia and sickle cell disease, the other two major haemoglobin disorders, carriers of β-thalassaemia were thus better able to survive malaria infections than individuals who were not carriers. The number of carriers increased significantly over the years in malaria-endemic regions of the world as large numbers of healthy individuals died as a result of severe malaria infection. Although malaria eradication programmes in recent years have led to a steep fall in the incidence of malaria in many parts of the world, tackling thalassaemia and other severe haemoglobin disorders nonetheless remains a considerable challenge.
Posted on: Wed, 08 Oct 2014 06:34:58 +0000
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