The individual will not contract malaria because the mutation in his or her genes quickly fights off the disease by changing the shapes and composition made-up of the blood cell so the parasites will not be able to survive in it.
The consequence of this is that because the individual's blood cells mutate and becomes deformed, becoming "moon-crescent or sickle-shaped," or even get spiked shaped. The blood cells then grow and become too big to pass through most blood vessels, mostly capillaries and veins; and clump together, forming a mass. The blood vessels, where this happens mostly is associated with the joints and the lungs. When this happens, the child or adults experience great amounts of pain in their joints and fingers, making it almost impossible for them to walk around. The joints then get swollen and red. Another condition is that the clump of mutated blood cells can travel to the vessels of the heart and cause a blockage. This is called a thrombosis. .
According to some research, the most common forms, or variations of Sickle Cell Anemia are homozygous (hemoglobin SS disease), heterozygous sickle cell hemoglobin C disease (hemoglobin SC disease), and the sickle Beta-thalassemia. Children and adults with homozygous sickle cell disease inherit a sickle cell (S) gene from each of their parents, and shows all the signs and symptoms of Sickle Cell Anemia, such as painful joints, chest pain, and kidney problems. Individuals with hemoglobin C disease inherit the S gene from one parent and a C gene from another. This means that they also show all the signs and symptoms of Sickle Cell Anemia. In some studies, it was shown that no normal hemoglobin (hemoglobin A) are produced by either one of the patients who has any one of the forms of the disease. .
With individuals born with sickle cell Beta-Thalassemia, the Beta [sup A] gene has mutated, and they are unable to produce the normal Beta [sup A] globin chain (Beta [sup b]) or a reduction in its production (Beta [sup +]).