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This synopsis will summarize the article titled Interactions of the malaria parasite and its mammalian host. The article aims to examine the parasite's relationship with the host. It particularly addresses the genetic aspects of the parasite-host relationship. It discusses how new research influences the knowledge we have about the relationship. It analyzes the ways that the parasite is able to continue to remain in the host so effectively.
Malaria is spread by the Anopheles mosquito when it injects Plasmodium after taking a blood meal from a human host. Sporozoites from the Plasmodium attack the hepatocytes of the liver. There are studies that have shown that the sporozoites pass through the skin and wander in the body until they reach a blood vessel that will allow them to reach the liver. The studies also propose that CD8+ T cells are prompted to react after the sporozoites are injected into the skin. These CD8+ T cells kill off the infected hepatocytes in the liver.
Sporozoites have to break the plasma membrane of cells to become an effective parasite. Three proteins have been discovered that aid in the sporozoite breaking the plasma membrane: sporozoite protein essential for cell transversal (SPECT-1), SPECT-2, and phospholipase. Sporozoites that do not have these special proteins are not able to travel around the body of the host. These lacking sporozoites are stationary on the dermis of the host. Those sporozoites that are not lacking the proteins are able to enter the blood stream. The circumsporozoite protein (CSP) covers the entire sporozoite. The CSP interacts with the heparin sulfate proteoglycans (HSPG) that cover hepatocytes. This interaction explains why sporozoites travel primarily to the liver of the host.
This article discusses a "switch from migration to productive invasion" of the parasite. After the sporozoite travels through many hepatocytes, it forms a parasitophorous vacuole. Torgler et al has demonstrated that the migration of sporozoites through different hepatocytes can induce inflammatory response that will kill the parasite. As mentioned before, sporozoites lacking SPECT are not able to migrate between hepatocytes; however, they do form a parasitophorous vacuole. Studies have shown that normal sporozoites invade slower than mutant sporozoites. This finding implies that the migratory nature of sporozoites can slow the onset of the actual infection in the host. There are many proposed causes of the switch to invasion such as: heparin sulfate proteoglycans, derivatives of potassium and uracil, and cell surface ligands.
As mentioned before, the sporozoites develop in the liver of the host. Recent research is giving us new insight on the relationship between Plasmodium and the host at the liver stage. When sporozoites lack genes that are upregulated in infected sporozoites (UIS3, UIS4), the hepatocytes they infect acquire protection from infection. Some in vitro studies have noted that UIS3 has a relationship with the liver fatty acid binding protein. A decrease in the liver fatty acid binding protein in turn causes a decrease of parasitic development. There appears to be a trend that lipid delivery is required for the liver stage of the parasite to develop effectively. The sporozoites develop into merozoites. A microscopic analysis of rodents infected with a species of Plasmodium demonstrated that when the merozomes, which are vesicles that hold the merozoites, leave the liver of the host whole. This is to protect against the parasite being killed by macrophages.
Merozoites are able to infect red blood cells. The invasion of merozoites into erythrocytes is executed in a set of steps. First, the merozoites attach to the red blood cell in a random fashion. The apical end of the merozoite ensures attachment to the red blood cell. The merozoite and erythrocyte form a tight junction and the merozoite is able to gain entry. The merozoite forms a parasitophorous vacuole and subsequently changes into a ring stage. The growing merozoites then go through DNA replication. Budding of the merozoites takes place and then they release exonemes which allow them to egress. The newly released merozoites find new surrounding erythrocytes and repeat the cycle continuously. Since red blood cells do not allow for endocytic and secretory pathways for parasites to take advantage of, Plasmodium utilizes other routes to help it grow parasitically. During the ring stage of the merozoite, a tubovesicular network is formed. This tubovesicular network increases the surface area of the parasite. The ring stage also solely relies on hemoglobin for its diet. A new study by Chang et al discusses how Plasmodium export element aids in exporting proteins like virulence factors into the erythrocytes. One protein the article mentions is a kinase called FIKK/TSTK. FIKK/TSTK is specifically encoded for parasites. Studying the exporting proteins can give us insight on how host restriction modification evolves, and moreover the relationship between parasite effectors and the targeted proteins of the host. According to researchers, red blood cell models are very important and can give us more knowledge about the proteins and how the Plasmodium develops, which can ultimately produce a more effective treatment for malaria.
Cerebral malaria has been the focus of several research projects. The researchers are looking to determine the genetic aspects of Plasmodium that control the factors of cerebral malaria. Heme oxygenase-1(HO-1) is the enzyme that determines whether a host will develop cerebral malaria. Recent studies have concluded that HO-1 was lower in mice that do develop cerebral malaria, and HO-1 was slightly higher in mice that are not susceptible to cerebral malaria. When HO-1 was completely silenced in unsusceptible mice, occurrence of cerebral malaria was significantly increased. Nitrous oxide and carbon monoxide have also shown to decrease incidence of cerebral malaria.
The research on malaria is very important on a global scale. Though malaria is no longer prevalent in the United States, it kills millions of people each year in many other countries. As a researcher myself, I believe that any new findings get us closer to a more effective treatment or cure for a disease. I found that the circumsporozoite protein interaction with proteglycans of hepatocytes to be very interesting. If possible, researchers should experiment a way to stop this interaction. Stopping this interaction could stop the invasion of the Plasmodium in the liver. In addition, work on mutating the sporozoites to lack SPECT will stop the Plasmodium from entering the body completely, which would be a tremendous accomplishment in malaria research.