The Heparin Sulfate As An Important Receptor For The It4

blood cells. The heparin sulfate has been suggested to be an important receptor for the IT4(var60) expressed by the parasite, once the red blood cell is infected (Angeletti et al., 2015). Using the ITvar60 rosetting variant the study’s objective to establish if binding to receptors occur through the use of a common structurally conserved binding site. The exact mechanism of binding remains unknown, however evidence narrowed down possible ways of neutralizing the infected red blood cells. The possibilities of controlling the infected red blood cells could be executed by directly blocking the binding site, through antibodies, or inducting a conformational change in the target protein once it is bound. Although Plasmodium falciparum is known†¦show more content†¦The endothelial barrier becomes leaky allowing parasitic infection to commence. Other symptoms of Plasmodium falciparum parasitic infection are anemia. Because of the infection of red blood cells, anemia is highl y likely once infected with the parasite. This is because of the lack of healthy red blood cells are circulating the human body. Examinations for a link between anemia and malaria have been conducted through the RSP2 surface protein. Through surface protein tagging, evidence has supported that the link occurs through sequestration, as larger amounts of red blood cells clump together (Layez et al., 2005). This unique molecular mechanism for destroying red blood cells was examined through the antibody response once anemia was witnessed. A chronic form of anemia can be observed. Anemia is common through the Plasmodium genus because all three species of Plasmodium infect red blood cells. Plasmodium falciparum not only can cause chronic anemia in most humans infected, but it can also be selective based on genes present in humans that can deter red blood cell infection. Another virulence factor to consider for this species is that of cytoadherence. During infection, this parasite releases adherence proteins, which incorporate themselves into the outer membrane of red blood cells. These proteins then attach to endothelial cell receptors in blood vessels preventing these infected cells from being cleared out by the spleen (Cholera et al., 2008). It is