Interactions of the Malaria Parasite and its Mammalian Host ( Synopsis ) . Malaria is the most common infective disease in the universe, which is responsible for killing more kids than any other individual pathogen. This unwellness begins when a mammalian host has been bitten by a mosquito transporting the Plasmodium parasites. These micro-organisms might be immobilized in the tegument, where they are attacked by the organic structure ‘s immune system or travel to the liver. In the liver, these parasites multiply, rupture the septic liver cells and are released into the blood channels of the liver, at which point the symptoms of malaria develop in the septic person. These parasites so infect, differentiate, and turn in the ruddy blood cells, where they finally break out of these cells to infect new red blood cells. In order to successfully forestall this deathly disease, scientists must carefully analyze the different developmental phases of these Plasmodium parasites every bit good as deeply investigate the interactions between the mammalian host and these parasites. Analyzing the function of the host ‘s skin immune response, the mechanisms of the tegument phase, liver phase and blood phase of these Plasmodium parasites, and understanding the oncoming and patterned advance of the terrible instances of malaria are some of the inquiries that must carefully studied in order to bring forth an effectual bar.
The Most Common Infectious Disease In The World Biology Essay
The first phase of malaria Begins when an Anopheles mosquito injects Plasmodium sporozoites into the tegument of the mammalian host. Inside the tegument ‘s cells, these parasites move in a random manner, where they disturb the plasma membrane of the tegument cells. ( SPECT ) -1, SPECT-2 and a phospholipase are some of the proteins that are indispensable for the random motion of these parasites in the tegument. Plasmodium parasites that deficiency these important proteins are non able to mobilise. The tegument may utilize different immunological responses to contend these parasites. Some of these sporozoites remain in the tegument where they are attacked by scavenger cells while other sporozoites are eliminated by the lymphatic circulation.
The sporozoites that will do the symptoms of malaria will come in the blood circulation and travel to the liver, where they will occupy and multiply inside hepatocytes. Upon making the liver cells, the sporozoites are covered with heparan sulphate proteoglycans ( HSPGs ) by the circumsporozoite protein ( CSP ) . This protein plays a major function in heightening the development of these parasites every bit good as downregulating the cistrons that express inflammatory response. The sporozoites so cross the sinusoidal cell bed of the liver cells, where they invade and produce the parasitophorous vacuole ( PV ) without upseting the plasma membranes of the host cells. A survey conducted by Torgler et Al. has shown that migration of Plasmodium sporozoites through liver cells can trip immune responses against these parasites. Therefore, the sporozoites must exchange from cell traverse to productive invasion manner, which leads to the formation of the PV. P36 and P36p/P52 are the two sporozoite proteins that are believed to hold a major function in the production of the PV, although the exact mechanism of the function of these proteins is still unknown.
The following measure includes the development of the Plasmodium sporozoites inside the PV membrane ( PVM ) . Recent surveies have indentified some of the indispensable proteins that are important in development of the Plasmodium sporozoites. UIS ( upregulated in morbific sporozoites ) cistron 3, UIS4, and Pb36p are the identified cistrons that encode for these proteins that are necessary in the development of these parasites. These surveies have besides shown that the parasites missing these cistrons are non able to encode these indispensable proteins which consequences in these parasites non being able to last and develop in the liver cells. In add-on, other surveies have shown interactions between UIS3 and the liver-fatty acid adhering protein ( L-FABP ) in vitro, where downregulating L-FABP has resulted in decrease of the growing of the Plasmodium parasites. These surveies indicate that lipid bringing is a important portion of the development of the Plasmodium parasites.
After the development of the Plasmodium sporozoites, the generation phase of sporozoites into 1000s of merozoites follows. The merozoites are contained within cysts called merosomes. Through a procedure known as emersion, the merozoites are released from the liver cells, assisted by cystein peptidases. A survey conducted utilizing Plasmodium yoelii-infected gnawers has shown that the merosomes leave the liver cells integral, which protects them from onslaught by Kupffer cells that are found in the liver cells. The symptoms of malaria are initiated when these merozoites finally reach the lung capillaries, where they enter the blood stream.
Plasmodium parasites are capable of occupying the ruddy blood cells quickly within few seconds. Merozoite surface proteins assist in attachment procedure of the parasites to the ruddy blood cells. There are besides transmembrane proteins that are involved in reorientation of the merozoites towards the erythrocyte surface every bit good as in incursion of these parasites into the ruddy blood cells. The red blood cell binding antigens ( EBAs ) bind to specific receptors on the surface of the merozoites, ensuing in efficient tract of invasion. A survey that was conducted in Kenya showed that the wild-type Plasmodium parasites use alternate tracts of invasion, which indicates the challenges scientists face in happening effectual vaccinums against this disease. Due to the fact that ruddy blood cells lack intracellular cell organs, the Plasmodium parasites are non able to obtain nutritionary beginning from their host. Therefore, the parasites must spread out their surface country through formation of a tubovesicular web ( TVN ) and curtail their diet to digestion of haemoglobin that is copiously found in ruddy blood cells, which consequences in the formation of the malaria pigment called hemozoin. A survey conducted by Spielmann et Al. investigated the early transcribed membrane proteins ( ETRAMPs ) which reside inside the parasitophorous vacuole membrane ( PVM ) . This survey revealed that these proteins are expressed in the developmental ring phase of the Plasmodium parasites inside the ruddy blood cells, while there are besides other proteins expressed in the liver phase of the Plasmodium life rhythm. In a turning stage known as the trophozoite, the merozoites asexually reproduce, multiply and spread out inside the PVM. This is followed by the merozoites releasing exonemes that consequences in the emersion of merozoites from the ruddy blood cells. The free merozoites continue to attach to new ruddy blood cells, in order to originate a new erythrocytic rhythm.
Symptoms of malaria scope widely from benign to severe, although terrible instances of this disease causes 1-3 million of deceases each twelvemonth. Cerebral malaria ( CM ) has been studied in research labs utilizing mice that have been infected with Plasmodium berghei ANKA in order to understand the mechanism that causes the oncoming of this terrible malaria. Although the oncoming and patterned advance of intellectual malaria is non related to the CD36 receptor, these surveies have revealed that the CD36 is the chief receptor that plays a major function in the infection of the ruddy blood cells by these parasites. Recent surveies have indicated that other factors such as chemokine receptors in the encephalon and histamine-mediate signaling contribute to the development of intellectual malaria in Plasmodium berghei ANKA-infected mice. Other surveies have shown that the upregulation of the host ‘s enzyme known as the haem oxgenase-1 ( HO-1 ) and the exposure to carbon monoxide ( CO ) suppresses the pathogenesis of intellectual malaria in these by experimentation septic mice. It is believed that these consequences occur due to the fact that CO binds to hemoglobin, which prevents hemoglobin oxidization and the coevals of free haem, a molecule which triggers the pathogenesis of intellectual malaria.
In decision, it is highly of import to carefully look into and analyze the different developmental phases of the Plasmodium parasites every bit good as to deeply understand the interactions between the mammalian host and these parasites in order to bring forth effectual bar methods against malaria. The surveies discussed supra examined the different mechanisms involved at different phases of the life rhythm of the Plasmodium parasites. The skin phase, the liver phase and the blood phase of Plasmodium parasites every bit examined on these surveies revealed the interaction between the mammalian host and these pathogens is important for the oncoming and patterned advance of malaria. These surveies further showed the assorted molecules, such as the receptors, surface proteins, transmembrane proteins, and enzymes that are involved for this interaction and in the life rhythm of the Plasmodium parasites. I believe more research should be conducted in the different phases of the life rhythm of these parasites in order to understand the exact mechanisms involved in the pathogenesis of malaria. I, specifically, believe the liver phase of Plasmodium parasites should be carefully investigated since the release of these parasites at this stage begins the symptoms of malaria. In my sentiment, the molecules of the parasites that are involved in infecting the liver cells and ruddy blood cells, such as the surface proteins, transmembrane proteins and enzymes should carefully be examined. I believe these surveies could take into effectual methods that could barricade, destroy, or extinguish these molecules and finally forestall this deathly disease of malaria.