Abstract
Immune evasion is a strategy used by pathogenic microbes to evade the host immune system in order to ensure successful propagation. Immune evasion is particularly important for the blood stages of Plasmodium falciparum, the causative agent of the deadly disease malaria tropica. Because Plasmodium blood stage parasites require human erythrocytes for replication, their ability to evade attack by the human immune system is essential for parasite survival. In order to escape immunity-induced killing, the intraerythrocytic parasites have evolved a variety of evasion mechanisms, including expansion of plasmodial surface proteins, organ-specific sequestration of the infected red blood cells and acquisition of immune-regulatory proteins by the parasite. This review aims to highlight recent advances in the molecular understanding of the immune evasion strategies by P. falciparum, including antigenic variation, surface protein polymorphisms and invasion ligand diversification. The review will further discuss new findings on the regulatory mechanisms applied by P. falciparum to avoid lysis by the human complement as well as killing by immune factors of the mosquito vector.
Highlights
With an estimated 214 million cases annually among 3.3 billion people at risk, the tropical disease malaria is a leading cause of death worldwide
Phagocytosis of the infected RBCs (iRBCs) is augmented by Ab-mediated opsonisation, which bind to plasmodial proteins that had been exported to the iRBC surface
The success of evasion of the human immune system by the malaria parasite blood stages depends on the large repertoire of anti-genetically diverse parasite proteins displayed on the surfaces of merozoites and iRBCs
Summary
With an estimated 214 million cases annually among 3.3 billion people at risk, the tropical disease malaria is a leading cause of death worldwide. During erythrocytic schizogony, which takes approximately 48 hours for P. falciparum, a single merozoite grows from the ring to the trophozoite stage, eventually resulting in a schizont containing 16 - 32 daughter merozoites These are released into circulation upon erythrocyte rupture and can each infect new erythrocytes to begin the cycle again. Phagocytosis of the iRBCs is augmented by Ab-mediated opsonisation, which bind to plasmodial proteins that had been exported to the iRBC surface These antigens are highly polymorphic and undergo clonal antigenic variation, meaning that effective opsonisation may only develop after many and varied malaria infections [13] [14]. We focus on what is known about the underlying molecular mechanisms underpinning complement evasion in falciparum malaria and highlight the latest findings and prospects of this interesting area of research
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