Malaria Parasite’s Immune Evasion

Introduction
“Malaria parasites are major human pathogens annually
associated with 300 million to 500 million clinical cases worldwide and 0.5
million to 3 million deaths, mostly among children under the age of 5
years living in sub-Saharan Africa” (Carter). Malaria is caused by a blood
borne infection by protozoan parasites of the genus Plasmodium, which TABLE 2.   Relative rosette-forming capacities of blood group A and blood
are transmitted from one human to another by female Anopheles group O RBC
mosquitoes. Four species of the plasmodium parasite can infect humans
(Fig.1): the most serious forms of the disease are caused by Plasmodium
falciparum. Malaria caused by Plasmodium vivax, Plasmodium ovale and Conclusion
Plasmodium malariae cause milder disease in humans that is not • Earlier data suggests that glycans are common rossetting receptors in many P.falciparum strains
generally fatal. Molecular genetics reveal that P. falciparum is very • Data from study suggests that all P.falciparum strains have the potential to use another receptor
confined to ABO blood group system
closely related to malaria parasites of chimpanzees; while the three
• Results show influence of ABO blood group type on rosetting
remaining species of human malaria parasite: P. malariae, P. ovale, and • Red blood cell polymorphisms also affect rosette formation
P. vivax fall under a single clade that includes all mammalian malaria • Differences in antirosetting effect of immune sera between isolates from group O hosts and
parasites. P. falciparum, causes the most severe infections and nearly all group A and B hosts reflect differences in strength of rosetting binding mechanism
• Show that A and B antigens are determinants for rosetting in P. falciparum
malaria-related deaths, and has been characterized in areas of high • Evidence for two different acting receptors for PfEMP1-mediated rosetting
endemicity in Africa. In my poster discussion I am going to focus on the • P. falciparum chooses different glycan interactions with the red blood cell surface for rosetting
P. falciparum strain of malaria, specifically looking at various antigen FIG. 1. Phylogeny of the malaria parasites of humans and of some other • Approach for creating vaccine must focus on rosetting ligand providing multiple targets where
binding proteins and concluding with future potential therapeutic blood group preference of the parasite in combination with blood group of that patient may be
related malaria parasite species. determinant factors
strategies derived from these various antigen binding receptors.
There is a great diversity of malarial surface antigens which is
one of the main reasons why clinical immunity develops only after
repeated infections with the same species over several years. Antigenic
diversity has a dual origin. One is the classical genetic mechanism of
nucleotide replacement and recombination that creates polymorphism,
the existence of genetically stable alternative forms of antigen-coding
genes. The second mechanism is antigenic variation. This is a clonal
lineage of parasites which express successively alternate forms of an
antigen without changes in genotype.
Previous studies conclude that the malaria parasite P.
falciparum utilizes molecules present on the surface of unifected red
blood cells for rosette formation. Rosetting formation is clusters
consisting of a cell (usually a lymphocyte) surrounded by antigenic cells.
The rosette-forming cell may be an antibody-forming cell, a memory cell,
a t-cell, or a cell bearing surface cytophilic antibodies. Rosette formation
can be used to identify specific populations of these cells.
References
Barragan, Antonio. Kremsner, Peter G.Wahlgren, Mats and Carlson,
“The P. falciparum erythrocyte membrane protein 1 (PfEMP1), a FIG. 2. Rosette disruption by immune sera in relation to ABO blood Johan. Blood Group A Antigen Is a Coreceptor in Plasmodium falciparum
member of a family of high-molecular-weight polypeptides encoded by group. Nine samples of immune serum from healthy individuals, six of Rosetting. Infect Immun. 2000 May; 68(5): 2971-2975.
blood group A and three of blood group B, were tested for
the var genes, has been identified as a rosetting ligand. Various host
antirosetting activity on isolates from hosts of blood group A, B, or Carter, Richard and Mendis, Kamini N. . Evolutionary and Historical
receptors on the surface of uninfected RBC have been proposed, O. Antirosetting activity (percent inhibition of rosetting) is depicted in Aspects of the Burden of Malaria. Clin. Microbiol. Rev., Oct 2002; 15: 564 - 594.
including ABO blood group antigens, CD36, CD35, and heparan sulfate a five-level grey scale as indicated. Two serum samples from
(HS) or HS-like molecules” (Barragan). However there is no evidence nonimmune Swedes (ni1 and ni2) were used as controls.
about the contribution of different receptors in rosetting and there natural
states.
This study focused on the utilization of ABO blood group
antigens for rosette formation. Clinical isolates were used to emphasize
the antirosetting effect of hyperimmune sera in relation to the ABO blood
group and to examine the relationship of A antigen to the rosetting
phenotype.

FIG. 3. Binding of A antigen to surfaces of parasite-infected

erythrocytes. (A) A antigen conjugate was allowed to bind to a living
culture. The pRBC were counterstained with ethidium bromide and
visualized by UV microscopy. (B) Sensitivity of rosetting and A antigen
conjugate binding by pRBC of FCR3S1 cultures to trypsin treatment as
indicated in Materials and Methods. (C) Competition of A antigen
conjugate binding to living cultures by A-trisaccharide and H-
disaccharide. All results shown are means SDs (error bars) from three
separate experiments.

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