Malaria is one of the infective diseases caused by protozoon Plasmodium species. It is a vector-born disease and transmits by septic Anopheles mosquitoes to human. Surveies shows that kids are more affected comparison to grownups. The common symptoms include febrilities and icinesss. The experiment on life beings and new intravital imagination engineering allow scientists to analyze host interactions at molecular and familial degree. Scientists conducted experiments to analyze how the Plasmodium parasite & A ; acirc ; ˆ™s distinguishable life rhythm phases between mosquitos to mammalian host, sporozoites to merozoites, tegument to red blood cells and cell acknowledgment proteins play of import function in developing malaria.
In the experiment, a mouse was infected with Plasmodium berghei. The mouse helps to detect the activity of four phases ; from tegument to liver, development of merozites in liver, entry into ruddy blood cell, and development indoors red blood cells ( silvie et Al. 4 ) . In the first phase, sporozoites signifiers of Plasmodium that nowadays in mosquitoes enter in to clamber when they bite to mammalian host. Surveies indicated that merely few of sporozoites migrate to liver cell. Some sporozoites that stay in dermis bed of tegument can destruct by phagocytosis or activation of CD8 and T cells if they enter into lymphatic system. The three proteins SPECT-1, SPECT-2 and a phospholipase are responsible in migration of sporozoites from tegument to liver cells.
The surface circum-sporozoites protein ( CSP ) on the sporozoites and heparan sulphate proteoglycans ( HSPGs ) on liver cells initiate the cell acknowledgment. At this point, sporozoites form PV ( parasitophorous vacuole ) composite and invade liver cells without destructing plasma membrane. However, survey suggests that mechanism of adhering to host receptors or activation by cellsingnal has non been clear yet.The 2nd phase is the development of merozoites in liver. These phase besides known as a soundless phase because host immune system does non acknowledge the rapid turning merozoites before they enter into ruddy blood cells. Harmonizing to the experiment in vitro, the upregulated in morbific sporozoites gene3 ( UIS3 ) and liver-fatty acid adhering protein ( L-FABP ) are necessary to organize merozoites. Even though, relationship between UIS3 and L-FABP is non known, it reduces the parasite growing without ordinance of fatty acids.
The mature merozoites are bounded with merosomes released from liver cell to blood watercourse by egress procedure. The survey based on intravital microscopy point out that merosomes protect merozoites from kupffer cells, therefore prevent phagocytosis. Kupffer cells are macrophages that are present in liver cells and activate during infection. Based on cistron and protein study, around 2000 active cistrons and 800 proteins are involved in parasite development at the liver phase ( Silvie et al 4 ) .
The 3rd phase is entry of merozoites into ruddy blood cell. A series of receptor-ligand interactions is necessary in attachment procedure between merozoites and red blood cells even though procedure occur rapidly. Experiment based on antibodies inhibiter from single exposed to malaria, show that it prevents peculiar invasion tract of parasite. Transmembrane protein apical membrane antigen1 ( AMA1 ) , can aim by antibodies to forestall invasion of parasite to red blood cell. EBA175 and EBA 181 are erythrocyte binding antigens are present in parasite and binds to glycoprotein of red blood cells of host.The Forth phase is development of merozoites inside ruddy blood cells.
Once merozoites enter into ruddy blood cell, they form pealing phase. At this phase, they replicate by budding procedure. Exonemes play of import function in emersion of merozoites.
These septic merozoites can attach with new ruddy blood cell quickly and get down new rhythm. The recent proteins surveies discover that 592 and 644 are soluble membrane proteins in human ruddy blood cell and ETRAMPs ( early transcribed membrane proteins ) that located on PVM in parasites play of import function in parasite development.Scientists use mouse that was infected by Plasmodium berghei as a theoretical account to analyze intellectual malaria ( CM ) . The survey showed that histamine mediated signaling, chemokine receptors, dendritic cell and T cell responsible for developing CM. However, enzyme that catalyzed haem oxygenese 1 ( HO1 ) in host prevent CM, neuroinflammation and encephalon microvasculature congestion.
Recent survey point out that HO1 ordinance is of import in liver phase development and red blood cell of parasite in malaria ( Silvie et al. 4 ) .In decision, scientist found other factors played of import function in malaria development beside merely the familial footing. Since Plasmodium parasite can last in both liver and blood cell, interactions of parasite in host are regulated by different proteins or ligand at specific degree. Among these experiments of different phases, the 3rd phase experiment is the most of import. From this experiment, scientists can carry on research to develop a malaria vaccinum.
To destruct malaria parasite before they can come in into ruddy blood cells, AMA1 antigens can be targeted by antibodies. However, the farther item survey needs to concentrate on the soundless phase of malaria parasite that does non recognized by host immune system.