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Plasmodium Inside The Mammalians Body Development Biology Essay

Development of plasmodium inside the mammalians’ body depends on the host species. The mosquito has to bite the host body twice in order to be able to infect the victim successfully. Adaptation occurs through few interactions between the parasite and the host. Plasmodium lifestyle ranges within stages of Sporozoite and merozoite; moreover, in the first step, the intradermal sporozoite injection initiates the infection as it enters to the liver cells. The symptoms of getting infected are shown by the body as chills and fever that lead to reducing the power of immune system. As a result, plasmodium parasite can get into the red blood cells to increase the number of parasitic divisions to be able to destroy the red blood cells.

As recent findings suggest, cellular and molecular mechanisms of the cells under genetic studying and imaging techniques perfectly show the interaction between the parasite and the host cells. Based on vivo models and new technologies, fluorescence views and intravital images of the parasite and the host cells prove the power of this deadly protozoan to human, especially, children. Infection to malaria always initiates as the plasmodium sporozoite enters the skin, which then travels to the liver as well as the RBCs; However, most of the time, skin itself is a barrier to fight the infection by production of phagocytes as well as the body immune system response. Also, the CD8+ T- cells of immune system are there to eliminate the infection in lymph nodes before getting into the liver. By studying this pathway, researchers found out that sporozoite can enter the blood stream and the liver cells by the interaction of circum-sporozoite protein (CSP) and heparan-sulfate proteoglycans (HSPGs) on the liver cells. At this point,

sporozoite is able to switch its traveler form to a productive invasion form in which can migrate through hepatocytes in a much faster progressive way to the liver.

Based on Torgler findings, use of genetically attenuated parasite (GAPs) is proven on production of whole-vaccine type. More studying on this pathway by using subtracted cDNAs during sporozoite development showed some upregulation of the parasite in blood and the liver stage. As an over view of the molecular studying in erythrocytes and the redundant genes in malaria, during maturation of merozoite in liver and blood stages, the parasite uses different specific pathways to utilize its stability throughout the body. This molecular aspect of plasmodium life cycle has not yet been proven one hundred percent through scientific investigations.

By looking at the redundant genes in malaria, the merozoite can attach to the surface of the erythrocyte by merozoite surface protein (MSPs). Then, the transmembrane protein, apical membrane antigen 1 (AMA-1) reorients the attachment to form a parasitophorous vacuole. Some of these specific membrane antigen proteins such as EBA 140 or EBA 175 bind to glycophorin C and A receptors on the cell that cause complex pathway of activating other receptors to bind to the merozoite protein. At this point in the body, instead of activating gene expression of the fight response to the foreign parasite, the entry of the merozoite to the cell progressively is maintained. This invasion pathway is proven in studies done on wild-type plasmodium in Kenya.

Production of this pathway by malaria in the host body can be blocked by use of inhibitory antibodies or the vaccine. However, malaria has become adapted to some of

these antibodies in a way that they can interact with receptor-ligand of the host cell membrane and become part of it, as it was mentioned earlier. Researchers found out that because mature red blood cells lack organelles, they are in advantage of being used by the parasite; moreover, they can be used as a nutrition source for the parasite to develop and grow in a faster pace.

As we know, erythrocytes do not show any antigens on their surface; therefore, the only way to avoid the formation of ring stages in RBCs is to restrict the dietary supplement of hemoglobin by using the remodeling factors. From the rodent models of malaria and experiments done on mice, the model of developing cerebral malaria (CM) is determined, which proves that in model animal, ANKA-infected mice, specific receptors such as Chemo-kine receptors in the brain and T cell receptors are required. Further investigation shows that host’s rate-limiting enzyme in catabolism of free heme (HO-1) can degrade the heme and generate iron and CO; however, this normal function of the enzyme is progressively decreased in the infected mice. Since heme oxygenase (HO-1) is a host molecule that controls the coexistence of the plasmodium infection and the host cells, it is important for scientists to keep this molecule under control for further investigation on the interaction of the malaria life cycle and the liver stages of development.

Critical points of this article represent the importance and improvement of human knowledge in investigating malaria parasite and plasmodium life cycle. Looking at details of the research done on mice as a model of studying as well as human cases in Kenya, researchers have gained enough evidence to draw the plasmodium life cycle and infection

pathway. The challenge is to overcome the plasmodium division pace inside red blood cells as well as knowing how to prevent the correlation of the plasma membrane receptors in liver cells with malaria merozoite. Specifically, this amazing finding from the experiments performed on mice can help researchers to differentiate between specific membrane receptors A and C to interact with EBA 140 and EBA 175 for the plasmodium initiation pathway.

By reading this article, every person is definitely going to be amazed by how much science has been improved that every little detail of this complex pathway has been diagnosed by scientists from the initiation part to the upregulation part of the life cycle. Moreover, it’s amazing how scientists are able to distinguish between microscopic receptors needed for the plasmodium engagement to the membrane in liver cells.


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