Malaria is a vector-borne infectious disease and is very deadly, especially to children. In fact it is the main killer in children comparing to other pathogens. The symptoms of fevers and chills occur during the time where the Plasmodium parasite is fastly replicating inside the red blood cell. When the Plasmodium sporozoites carrying mosquito injects the pathogen into the skin of the human host, it will then travel to the liver. Not all the pathogens will reach the liver because a lot of them will remain near the injection site. According to a study, sporozoites can remain in the skin for a very long time before migrating to the liver. What happens to those sporozoite that does not reach the liver or bloodstream are either destroyed by phagocytes or degraded in the lymph node if the pathogen happens to enter the lymphatic circulation.
The Plasmodium sporozoites that do make it to the liver will develop inside hepatocytes. The ability to migrate depends on three parasitic proteins: SPECT-1, SPECT-2, and a phospholipase. Once sporozoite reaches the liver, it will switch from migrating mode to invasion mode. It will then form a specialized compartment called parasitophorous vacuole (PV). A study shows that migrating through hepatocytes during sporozoite infection can cause severe effect to the parasite development depending on the NF-kB activation. An interesting study by Coppi et al shows that concentrated sulfated HSPGs in the liver gives signals to switch to infection. Another study also suggests that there can be several pathways that are involved in hepatocyte receptors allowing sporozoite entering.
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During the liver stage development, the Plasmodium spotozoite grow and increase into thousands and thousands of new merozoites. It then will be release from the hepatocytes and into the blood stream. The necessity for the parasite to develop normally involves UIS gene 3, UIS gene 4, and Pb36P. A study shows that down regulation of L-FABP will lead to the reduction of parasite development. Another study found that lipid delivery is very important for Plasmodium liver stages (LS) development because if there was a down regulation of the lipoprotein receptor, Scavenger receptor type B class I (SR-B1), it will hinder the parasite development in vitro. As soon as the merozoite reaches the blood stream, it will begin the blood-stage of infection.
Like Plasmodium, there are other apicomplexan parasites that have the ability to invade red blood cells at an enormous rate. Examples of such parasites are Babesia and Theileria. A study that was done involves inhibitory antibodies suggest that the transmembrane protein apical membrane antigen 1 (AMA-1) allows the reorientation of the apical end of merozoite towards the erythrocytes surfaces. Wild type parasites use alternative invasion pathways such as hierarchic organization of P/RHs and EBAs that allows competent entry. Yeoh et al demonstrate that specialized organelles such as exonemes is involved in Plasmodium compartimentalize that function in egress.
Once the merozoite is developing inside the red blood cell, it is very severe and life threatening. Red blood cells that are mature lack the standard biosynthetic pathways and intracellular organelles. An advantage for the pathogen is that red blood cells do not display antigens on their surfaces. But because there are no endocytic and secretory pathways it makes it hard for the parasite to take in host organelles for nutrients. A new diet limit will be in place because there is a lot of hemoglobin so it will have to expand the surface area by forming tubovesicular network (TVN). A study by Chang et al found that Plasmodium export element (PEXEL) functions as a cleavage and N-acetylation site.
The oomycetes in plant pathogen can translocate effector proteins to create infection using a similar mechanism like the kinases. A study on proteome reveals that there are 592 and 644 identifiable membrane associated and soluble proteins in uninfected human and miceâ€™s red blood cells. It concludes that from reticulocytes to old red blood cells require more proteins than expected. Studies that focus on the make up of PVM can help us understand the molecular interaction at the parasite-host interface. So Spielmann et al did a study that shows that early transcribed membrane proteins (ETRAMPS) form oligomers that confine to the microdomains suggesting thereâ€™s polarity of the parasite-host interface.
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Malaria is a detrimental disease that has a broad range of symptoms. The majority of the infected individuals will experience minor fever aches. The more severe malaria can cause one to three million deaths every year and is mainly in children. It can also bring about other syndrome such as severe anemia, acute respiratory distress and cerebral malaria (CM). Rodent models are great for studying severe malaria mechanism. It has especially been helpful understanding the development of cerebral malaria. Study shows that it is not favorable to delete Hmox1 or prevent HO activity because that can increase cerebral malaria occurrence. NO which is an inducer of heme oxygenase-1 (HO-1) prevents early cerebral malaria in mice. Another benefit is that if come in contact and inhale CO, it can also protect mice from cerebral malaria. Both HO-1 and CO put a stop to the disruption of blood-brain barrier, brain microvasculature congestion, and neuroinflammation. An important fact is that HO-1 controls the formation of the Plasmodium liver stage of infection and the formation of pathology during the blood stage of the infection.
The experiments and studies done are to help the community have a better understanding what is happening during an infection of malaria. The studies help others to visualize the mechanisms and see what is occurring in order to better understand it. These studies have a higher motive of eventually finding a solution to prevent and treat malaria. These studies are so important because it can save millions of lives. It really would be a significant highlight in modern science. I think the data revealed in these studies can help scientists slowly create a vaccine to treat and prevent malaria. The more study done the better to understand the disease to stop it before it infects. To me malaria is a deadly infection but with research and time, nothing is impossible with science.