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Plasmodium affects millions of people around the world. It occurs when the female Anopheles mosquito bites the human and injects the Plasmodium sporozoites into them. It causes malaria which kills hundreds of millions of people every year. (1) Because this disease is so dangerous this article wants to show the genetic basis of the parasite-host interactions through rodent in vivo models. The experiment will show the cellular and molecular processes of parasite-host interactions. They will help understand importance of the eukaryote red blood cells, cellular and immune functions, the target it infects, and how it feeds. This information could help answer the question on how to eliminate Malaria worldwide.
There was a study done that concluded that after injecting a human the sporozoites move around erratically in the skin until they find a blood vessel and enter blood circulation. It also showed that some don't " make it to the blood circulation and liver because they are eliminated by phagocytes."(1) There are also some sporozoites which "reach the draining lymph node and are destroyed. "(1) They inject in the CD8+ T cell which help get rid of parasites in the liver. This shows that the lymph node works to protect humans from Plasmodium.
The NF-ÎºB activation has an important effect on if the parasite survives in the liver of the human during the process of migration, through hepatocytes, during the sporozite stage. The molecular process from migration to invasion is not fully understood. It is also concluded that SPECT mutants, which do not transmigrate and form a PV, infect better than normal sporozoites. This observation shows the migration kills the infection and it would have to be turned off and form a PV to infect. There are also ligands the work together with cellular receptors which could help enter the hepatocyte plasma membrane and form the PV. The way hepatocyte receptors enter the sporozoite has not been figured out but it may have something to do with tetraspanin CD81 and cholesterol-enriched micro domains. There are also two sporozoite proteins P36p and P52 which may contribute to creating the PV but it is not known how they do it. It is very likely there are more sporozoite molecules involved during invasion of hepatocyte and they could help with creating vaccines for malaria.
Several Plasmodium proteins have been found that are needed for its survival. Parasites that do not have UIS (upregulated in infective sporozoites) gene 3, UIS4, and Pb36p are protected against re-infections and this could be a big step in use of these parasites to create a vaccine. "In vitro the UIS3 binds with the liver fatty acid binding protein (L-FABP) but this could not be found in hepatocytes."(1) But decreasing of the L-FABP causes the parasite to develop less. It is also shown that lipid development is important in the Plasmodium liver development. In vitro it was shown that down regulation of " lipoprotein receptor scavenger receptor type B class I (SR-BI)"(1) helped stop parasite growth. An interesting study done shows there are "2000 active genes and 800 protein genes in the process of P. yoelii liver stage."(1)
Our knowledge of molecular events in the parasite is known by biochemical and structural data. Experimental data is not viable in erythrocytes and only show unimportant genes in the parasite. The parasite attaches at the merozoite surface proteins (MSPs) and then studies show the "transmembrane protein apical membrane antigen 1(AMA-1) leads the next step."(1) These two steps cause the merozoite to penetrate its host.
There was a study done in Kenya that showed different invasion techniques used by wild-type parasites. People infected with Malaria can block specific invasion techniques but not different pathways which can be a road block for creating vaccines for multiple alternative ligands. This study shows co evolution of the "parasite-host cell receptor-ligand interactions."(1)
Red blood cells are the best model to show development of a pathogen. "There were two studies done that showed 592 and 644 proteins in non-infected human and mouse red blood cells."(1) This showed new to aging erythrocytes have more proteins than anticipated. This knowledge will help future studies show how the Plasmodium develop in the red blood cells. There was also a study done that showed early transcribed membrane proteins (ETRAMPs) help show the polarity of the parasite-host invasion. This can help show the complication of the parasite-host interactions and what causes growth in host cell.
The use of rodents as malaria models has been very useful in finding different things this disease does to the host and how it infects. This is a very complicated process which is made simpler by experimenting with the rodents. The receptors in the mice and mosquito are very similar which make it easier to examine how cerebral malaria occurs and its stages. It was found that exposure to inhaled CO protect mice from cerebral malaria. Experiments like this in mice make it very beneficial in finding a worldwide cure for Malaria.
In conclusion these experiments are showing the cellular and molecular processes of parasite-host interactions. They help understand importance of the eukaryote, cellular and immune functions, the target it infects, and how it feeds. This work is important because it can help us understand the disease in a way we wouldn't have been able to before. This could lead to helping find a vaccine for malaria worldwide. This data is also important because we are learning more in detail about the complicated steps of parasite-host invasion. I think the data is very interesting and educational. It told me things about Plasmodium I never knew before. It goes in great detail, with the data and experiments, about the parasite-host interactions. I would like to see them investigate more into what the disease does to the host red blood cells and if there is something we could do to prevent it from infecting them. I also would like to see if more investigation on Kenya studies about the wild-type parasites because we need a cure for it. They should also look into something we could do to attack the mosquito parasites proteins so they wouldn't be successful at passing the disease to the host. Overall the research was very well done and I hope this continues so we can eliminate one of the world's most dangerous diseases.
Silvie O, Mota MM, Matuschewski K, Prudêncio M. Interactions of the malaria
parasite and its mammalian host. Curr Opin Microbiol. 2008 Aug;11(4):352-9.
Review. PubMed PMID: 18644249.