Effects of Malaria on Sickle Cell Anemia Frequencies

Effects of Malaria on Sickle Cell Anemia Frequencies

The female anopheles’ mosquito is responsible for the spreading of malaria in human beings. Malaria is a disease which is caused by a parasite known as plasmodium. When one is infected with malaria, he or she usually experiences episodes of shaking chills and high fever. The total number of people affected by the disease every year averages to millions of people while of these hundreds of thousands die. For example, in 2018, the disease caused the death of about 228 million persons, while 405 000 succumbed to the illness (WHO par. 4). Most people who die from malaria are mostly young children in Africa.

The five kinds of parasites that can infect individuals with malaria are Plasmodium (P). ovale, P. vivax, P. malariae, P. Knowlesi, as well as P. falciparum (Talapko 1). According to Geleta and Ketema, a more severe form of the disease is experienced if the infected individual was bitten by a mosquito carrying P. falciparum parasite (1).

Sickle cell anemia is known to be one of the sickle cell disease disorders. It is a disease whose one of its risk factors is heredity. Notably, it can be passed from parents to their children. Sickle cell anemia affects the haemoglobin in the blood, causing the red blood cells to be warped and appear to form a crescent moon or sickle shape. This makes the body to have small healthy red blood cells in the body, causing the limited or insufficient supply of oxygen. Typically, red blood cells are rounded, flexible and pass through blood vessels easily. For sickle cell anemia’s case, the red blood cells are warped and look like sickles or crescent moon. When the warped red blood cells get in the way of smooth blood flow in the body, they often get trapped at small blood vessels blocking the movement of blood and oxygen from reaching other parts of the body.

People with this condition have (HbS) hemoglobin S, which distorts red blood cells sickle-shaped. Theoretically, those with dominant homozygous (HbA) and heterozygous (HbA HbS) genotypes survive. On the other hand, those with homozygous recessive genotype coding for sickle cell (HbS) show the symptoms of the disease and might have complications (CDC). In some cases, persons might die at a young age due to disease complications.

Some resistance is noticed to malaria from individuals having the sickle cell trait, this favours the survival of the host and supports the abnormal hemoglobin gene transmission. Inheritance of a single abnormal gene shields an individual against malaria. In contrast, heritage of a pair of abnormal genes offers no such protection and leads to the risk of sickle cell disease. Sickle cell anemia in Africa is not only influenced by malaria disease but also changes its manifestations.

The heterozygous advantage is that individuals who have only one copy of the sickle cell gene; HbA HbS tend to be more resistant to malaria than healthy individuals without the mutated gene pool (Chakravorty & Williams 48). This is because individuals containing only one copy of the sickle cell trait have misshapen red blood cells which prevent Plasmodium parasites from infecting a large number of red blood cells. Natural selection keeps typically harmful alleles. If a person carries a genetic disease, there are high chances that his or her children will likely get sick or die eventually (Xu & Thein). However, for the heterozygous individuals, they are more likely to survive than people without the disease allele.

The sickle cell trait will be noticed to spread to populations living in geographical areas where malaria is rampant since it helps in survival. This is why some genetic diseases are found to be universal.

Testing this selection theory in an experimental population which contains heterozygous individuals, HbS allele frequency and malaria. The heterozygous and malaria-carrying individuals will increase while homozygous HbA genotypes will decrease. Experimental population without malaria, the homozygous HbA genotypes will increase while the HbS allele frequency will decrease.

Methods

• Experimental methods were conducted under the supervision of Professor Trubl, he instructed us into comparing two assumptions done from frequency presence of HbA allele to HbS allele in 2 populations, one with malaria and one without, in the course of two generations.
• Simulation 1, an individual is represented by removing two alleles from the gene pool. Malaria presence is presented with a 50% chance of the individual contracting it. For Homozygous HbA genotypes this provides a 50% chance of survival, 100% for heterozygous genotypes to survive and 100 per cent mortality rate for homozygous HbS genotypes.
• Simulation 2, an experiment was conducted just as simulation 1, without the presence of malaria. 100% survival of homozygous HbA genotypes and heterozygous and 100% homozygous HbS genotypes will perish (Trubl).

Results

In simulation 1, this is an area with many female anopheles’ mosquitoes, from initial generation to 1st generation the HbS allele rose by 0.03 and 0.04 from the 1st generation to the 2nd generation.

From initial generation to 1st generation, HbA allele decreased by 0.03 and 0.04 from 1st generation to 2nd generation.

For genotypes, 0.07 was the rise of HbA HbS from initial generation to 1st generation and 0.08 from 1st generation to 2nd generation.

HbS HbS varied while HbA HbA decreased.

In simulations for HbS allele and HbA for generation 1/2, the standard deviation stayed the same in a population of 22 (in-sample size)

The chi-square table showed both populations were not hardy Weinberg equilibrium (Trubl).

Discussion

The presence of malaria is the one causing the selective pressure for the frequency of sickle cell allele, HbS, and this proves the hypothesis posed initially. This hypothesis is that malaria presence influences HbS allele frequency.

Individuals found to carry a single copy of the sickle cell trait develops sickle cell anemia. However, individuals are asymptomatic carriers. More so, the persons are highly resistant against malaria (Archer et al. 1); this explains the high-frequency prevalence of the mutation in areas where malaria is prevalent.

People from Mediterranean and Africa descent have the highest mortality rates from sickle cell anemia. Heterozygous genotypes have the lowest chances of mortality, even with the presence of malaria compared to non-carriers HbA HbA.

What seems to be protecting people against malaria is the carrier trait of the gene HbA HbS. This knowledge noted has helped given an understanding of how genotypes and alleles are passed down through generations in the said populations.

This work has provided a full understanding of genotypes and alleles and how diseases affect them. For example, a child born from one parent with the carrier trait results in the child being an asymptomatic carrier. In contrast, the child who has inherited from both parents is very vulnerable and will suffer from sickle cell anemia (CDC).

Sickle cell hemoglobin prevents of Plasmodium parasites from reaching many red blood cells or even taking hold to survive in the body following infection (Rozenbaum). Radically, the limitation to the parasite by sickle cells reduces the number of red blood cells being infected and thus protect against malaria.

In summary, the sickle cell trait is fatal; the heterozygous genotype is favoured by the selective pressures leading to an increase of the allele gene HbS. In the second simulation, a general decrease in the frequency of the gene allele HbS and there was no heterozygous advantage without malaria presence.