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Malaria is a protozoan disease that which is notorious and lethal. The article written by Olivier Silvie, details mechanisms of how the disease is transmitted and eventually affects individuals. The article also addresses the different stages of reproduction for the disease within its host. This paper will discuss the article's overall significance, its main points, and studies that were conducted throughout the paper.
Synopsis of the data
Malaria is recognized as a disease that's capable of inflicting detrimental symptoms upon its host. The process of the disease starts out by merosomes being transmitted into the liver by an infected mosquito known as an Anopheles mosquito. Merosomes are proteins that are made of merozoites. Those proteins are used to impel the merozoites inside red blood cells. Once merozoites are inserted into the skin, they continue to move in an unsystematic way until a blood vessel is reached. Once inside an erythrocyte, the merozoites are spread during blood flow.
SPECT-1, SPECT-2, and a phospholipase are all proteins that are needed for the sporozoites to pass through cells. After reaching the blood circulation, a special protein known as CSP (circum-sporozoite protein) is used for further movement into the liver. While inside the liver, sporozoites move from the traversal stage into an invasive stage. This process results in the parasitophorous vacuole (PV). The PV formation is critical. Within the PV, sporozoites transform into early liver stages. P36 and P36p/P52 are two proteins that are recognized as facilitators during formation of the parasitophorous vacuole.
After the process of the invasion, sporozoites of the Plasmodium increase and develop into numerous fresh merozoites. These merozoites are enclosed in the PV membrane (PVM). They are retained in the PVM until freed into the bloodstream by hepatocytes. Hepatocytes are described as skin cells made from the liver (Webster, 2010). During the liver stage, the understanding of how these molecules interact is not fully known.
Within this article, it has been postulated that several proteins are essential for ordinary maturation of the parasite. The proteins are known as Pb36p, gene 3, UIS4, and UIS. Without these particular proteins, it has been noted that parasites will discontinue progression into an established hepatocyte. It is also stated that without these proteins, parasites are able to refuse an Anopheles mosquito that has been infected with a disease. This proposes a way for scientists to invent prospective vaccinations.
Intravital microscopy was a study that was performed in rodents to show the exiting of merosomes out of the lung. This study showed that merosomes are whole upon egress. Another study showed the use of the protein UIS3. This study was performed in the laboratory. Results showed that a decrease or absence of this protein inhibited parasite progression.
Further studies are needed to reach a more thorough conclusion of the mandatory life cycle of the Plasmodium. Not only can the Plasmodium enter into the erythrocytes, but it has multiple choices about where exactly it can and will go. These options have been found to be mainly utilized by unordinary parasites. The process of replication inside red blood cells occurs through a series of steps.
The first step begins by merozoites searching for a red blood cell. Once an erythrocyte is located, attachment is imposed by the top end of the merozoite aligned with the red blood cell. A special transmembrane protein known as AMA-1 (apical membrane antigen) is responsible for assisting the merozoite in the proper orientation. Once this occurs, invasion is initiated. Concurrently, PV formation occurs. In the completion of invasion, the merozoite converts into a ring. The stage proceeds into DNA replication of merozoites and buds off. Lastly, merozoites attach to neighboring red blood cells which begins a new life cycle.
The life cycle of the Plasmodium inside erythrocytes is interceded through the host targeting signal or the Plasmodium export element (PEXEL). A study showed that this particular protein complex has been found within multiple parasitic proteins. Effector proteins have been found to be excreted through this signaling complex. Kinases are an example of effector proteins that have been found to be associated with the host targeting signal. Studies of this system are used for elucidating the restriction of the host as well as the parasite effector and host cell protein existing simultaneously.
Further studies have taken place that shows the importance of RBCs (red blood cells) and membrane associated proteins. Many more proteins are suspected within the process of RBC maturation. This knowledge gives scientists a way to further study the Plasmodium developmental process. It also allows for studies on host factors that are essential for RBCs.
Responses to this lethal illness have shown variations. The main individuals that are susceptible to further diseases are children that have never been exposed to this type of sickness. In this case, children can develop diseases such as cerebral malaria (CM), brutal anemia, and acute respiratory suffering. Studies have been performed on mice that show signs of cerebral malaria. One of the main findings was with the proteins of HO-1 and CO. HO-1 has been found to be down-regulated in mice that contracted CM. CO works with HO-1. Consequently, mice that were exposed to CO did not contract the disease.
Within this article, Olivier Silvie speaks on the way CO prevents inflammation in the brain. An upregulation of HO-1 was found to prevent cerebral malaria. Studies have confirmed that once sporozoites have been introduced into the host cell, HO-1 is upregulated. HO-1 is an important molecule that controls the development of the Plasmodium life cycle.
In conclusion, the article features information on the Plasmodium life stages. The proteins and the different mechanisms involved provide a major hallmark for further studies to be conducted. This information can be used as a way to inhibit Malaria via preventative methods. Even though the information provides behaviors of the disease and its lifecycle, it was difficult to understand. Some of the content seemed incomplete in explanation. The structure of the paper provided valuable knowledge. However, a simpler way to present the data and results would be more efficient.