Sickle Cell Anemia In Sub-Saharan Africa

To the majority of the population in the United States, malaria feels more like a myth than a threat. Vaccinations and medicine targeting the disease are reserved for the venturesome travelers who dare to enter malaria-endemic regions. Unfortunately, for 3.2 billion people across 106 countries and territories--malaria is a very real threat, and often times fatal. Typically, malaria is found in warmer regions around the equator. However, some areas are hit harder than most. Of the 214 million clinical cases of malaria and 438,000 deaths from the disease in 2015, 88% of the cases and 90% of the deaths were from Sub-Saharan Africa. Much of these deaths could have been easily preventable with modern medicine; but unfortunately, most of those who

Hemoglobin A, an oxygen-carrying protein in blood cells, becomes abnormal once a point mutation occurs on chromosome 11. The mutation causes the sixth amino acid of the protein to change from glutamine to valine, resulting in the abnormal hemoglobin S. An autosomal disease known as sickle cell anemia is caused by having homozygous recessive alleles of hemoglobin S. Hemoglobin S form stiff strands within the blood cell which results in the sickle, or crescent shape of the diseased blood cells. Unlike healthy blood cells, the sickle cells are not flexible and often stick to vessel walls, causing painful blood clotting or a vaso-occlusive crisis. Patients can also suffer from joint pain, hematuria, jaundice, and dizziness. The life expectancy of sickle cell patients in North America, the Caribbean, and Europe is mid 40’s. However, approximately 240,000 of the 300,000 people born annually with sickle cell anemia are born in Sub-Saharan Africa and around 50% to 80% of those sickle cell anemia patients die before the age of five. The great discrepancy in life expectancy can be pointed to the poor healthcare infrastructure in the majority of Sub-Saharan African

In the healthy uninfected cells, actin filaments accumulated under the cell’s membrane. The infected cell showed that the parasite steals the actin and constructs an a bridge to move adhesin, a parasite-made protein to the surface. Adhesin causes the blood cells to stick to the cell wall--causing a microvascular inflammation. Unlike ‘normal’ cells, the actin bridge is not connected to the adhesin reservoir and the transport vesicles are floating in the cytoplasm. In order to survive, the parasite must rebuild the bridge. However, when the abnormal hemoglobin reacts with oxygen, ferryl hemoglobin is produced. While the actin proteins would normally polymerize to form the bridge--the ferryl hemoglobin obstructs it by preventing the proteins from polymerizing. While those heterozygous for sickle cell are considered “malaria-resistant,” they are able to contract malaria. However, their chances of dying from malaria are significantly lower. A study in Uganda showed that heterozygous children aged 1-10 were protected from the infection of the red blood cells, high concentrations of parasites in cells, and symptoms of malaria. However, those homozygous for sickle cell anemia have a decreased chance of surviving after contracting malaria because their susceptibility to infections is increased and their immune system cannot fight the