Final answer:
Individuals with the HbA HbS genotype, or sickle cell trait, are resistant to malaria because their red blood cells, which can take on a sickled shape, create an environment that inhibits the malaria parasite. This genotype is a common genetic adaptation in areas where malaria is prevalent.
Step-by-step explanation:
Individuals with the HbA HbS genotype do not develop malaria because the presence of the sickle cell trait confers resistance to the malaria parasite. Heterozygotes, having one normal hemoglobin gene (HbA) and one sickle cell gene (HbS), possess a unique blood chemistry that inhibits the malaria parasite's lifecycle.
When a person carries only one copy of the sickle cell gene, they typically do not exhibit the full symptoms of sickle cell anemia; however, their red blood cells can acquire a sickled shape under certain conditions. This change in shape and the altered properties of the red blood cells provide a hostile environment for the Plasmodium parasite that causes malaria, thereby granting a certain level of natural protection against the disease. Luwi, depicted in the scenario, would be resistant to malaria as a carrier of the trait, while Sena, lacking the gene, would not have this protection.
The sickle cell gene is particularly common in regions where malaria is endemic. This genetic adaptation is prevalent in sub-Saharan Africa, the Middle East, and India. The protection offered by the heterozygous condition (HbA HbS genotype) explains why the sickle cell allele remains in the population in these areas, despite the health risks associated with having two copies of the gene.