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Plasmodium is considered the most deadly protozoan to the human race. The pathogen it causes, malaria, is thought to produce the highest fatality in children than any other single pathogen. Researchers are making great efforts to understand the interactions between host and parasite cells through cell signaling and recognition, the gaining of nutrients, and the seizing of host cells because of the importance of medicinal potential in these areas. Plasmodium has a very complex life cycle and has several stages in the mammalian host. Once the female Anopheles mosquito injects its proboscis into the dermal layer, the sporozoite form of the pathogen is injected into the skin. The sporozoite cells migrate through the host through disruption of the plasma membrane of the cells. This pathogen is successful at making its way through the cells because it has three surface proteins that help them transverse through skin cells. The three proteins are (SPECT)-1, (SPECT)-2, and phospholipase and if any sporozoite does not have (SPECT)-1 or (SPECT)-2 there will be a build up of cells in the skin which will be recognized by immune system cells. The sporozoite can typically stay in the skin for extended periods of time until they make there way through the dermal layer to enter into the blood circulation. Not every sporozoite moves on to the next stage of the life cycle; some parasites are exposed of by the immune system. These extended exposures of plasmodium to the immune system are thought to provide a protective immune response for future exposures. When sporozoite are able to migrate into blood circulation, they make their way to the liver tissue. Once the sporozoites are able to enter into the hepatocyte cells they begin a part of the cycle called productive invasion. Once in the hepatic cells the parasite will form specialized compartments that aid in the production of merozoites. This process is usually takes place after the sporozoite has moved through several hepatic cells. This phenomenon is not fully understood but is thought to occur to avoid damaging effects of an inflammatory response from the initial invasion. When the sporozoite has successfully reached the liver cells undetected by the immune system, it begins the maturation process where the parasites in the hepatic cells start rapid cell division forming merozoites in the specialized compartment called the parasitophorous vacuole. The molecular interactions and the molecular events that occur in the liver stage needs much more research. Cell signaling proteins and ligands are thought to play a significant role in down regulating liver cell inflammation and by making the conditions right for development. It is thought that there are many mechanisms and strategies of the liver cells that make them successful at enhancing nutrient retrieval and survival capabilities. The merosomes are derived from the host cell membrane and are released from the hepatocytes. Cystein proteases are thought to signal or moderate the release of the merozoites into the blood circulation, to migrate to the lungs. This process of egress it thought to up regulate a class of serine proteases that help release merozoites from the merozomes. There is an analysis that is used to view in vitro occurrence of rodents and is called intravital microscopy. When the merosomes are leaving the liver cells they are mostly intact proving to be an excellent tactic for evading the macrophage liver cells called Kupffer cells. This group of cells leave the liver as a membrane shielded merosome and make their way to the lungs where they rupture in the microvasculature releasing merozoites to begin the blood infection stage of the malarial life cycle.
There are many questions in the plasmodium life cycle. Many researchers have questions regarding the mechanisms of how the parasites enter the hepatocyte cells through hepatocyte cell receptors. Also, its not fully understood all the cell signaling required to initiate the formation of parasitophorous vacuole. In the larger picture, the main problems with finding a vaccine for malaria is not fully understanding the cell to cell interactions, mechanisms, and signaling that occurs to help this parasite completes all the necessary life cycles. One of the posed problems is the relatively silent existence of the parasite in the human host, especially in the liver stage. Another huge problem researchers are having is all of the alternate ligand options that the parasite utilizes. Multiple cell receptorââ‚¬"ligand interactions between the host and parasite that provide many parasite invasion pathways have shown to be blocked by malaria exposed individuals as time increases. This is a problem with created vaccines that target these interactions because to shear number of ligands that are capable of being an alternative to the once being vaccinated for. Most of the stages that malaria go through present a question that researchers continually try and answer. When the merozomes are in the blood stream, they enter the red blood cells. The problem with them traveling by RBC to the lungs is that they go undetected by the immune system because they do not exhibit antigens on the surface of the cell.
In future research, the investigation of sporozoite molecules involved in the invasion process should explored more intensively for possible vaccinations. This article addresses the possibility of UIS3 protein as a potential attenuated vaccine. Apparently, there has been extensive research on this protein and they have found that this protein up regulates L-FABP, which causes significant reduction in parasite development. The article didn't address any problems with this actually being a vaccine. There needs to be in vitro testing on this protein for possible application as a vaccine. They also talked about how mice have been very helpful in understanding different mechanisms that take place throughout the life cycle, but they should also look into using different model organisms like monkeys. Another topic that was interesting was the role of heme oxygenase. In mice it showed to help prevent cerebral malaria which is caused by a different strand of Plasmodium. While its independent of the human infectious malaria, the test provide insight to future research in the interaction of various enzymes in the human pathogen.