Abstract

Malaria is the most deadly parasitic disease, affecting hundreds of millions of people worldwide. Malaria parasites have been associated with their hosts for millions of years. During the long history of host-parasite co-evolution, both parasites and hosts have applied pressure on each other through complex host-parasite molecular interactions. Whereas the hosts activate various immune mechanisms to remove parasites during an infection, the parasites attempt to evade host immunity by diversifying their genome and switching expression of targets of the host immune system. Human intervention to control the disease such as antimalarial drugs and vaccination can greatly alter parasite population dynamics and evolution, particularly the massive applications of antimalarial drugs in recent human history. Vaccination is likely the best method to prevent the disease; however, a partially protective vaccine may have unwanted consequences that require further investigation. Studies of host-parasite interactions and co-evolution will provide important information for designing safe and effective vaccines and for preventing drug resistance. In this essay, we will discuss some interesting molecules involved in host-parasite interactions, including important parasite antigens. We also discuss subjects relevant to drug and vaccine development and some approaches for studying host-parasite interactions.

Highlights

  • The mechanisms for generating pir gene diversity are expected to be similar to those of var genes, including amino acid substitutions at specific antigen epitopes in response to immune pressure and the generation of new recombinant genes through genetic recombination as well as microhomology-mediated end joining (MMEJ) mediated somatic deletion, insertion and translocation

  • The results suggest a reciprocal selection between malaria parasites and mosquito vectors and local adaptation of the parasites to mosquito species in different environments

  • In a follow-up study using mRNA isolated from the spleens of infected mice 24 h pi, many host receptors including Toll-like receptors (TLR), retinoic acid-inducible geneI-like receptors (RLRs), G-protein coupled receptors (GPCRs), and olfactory receptors (ORs) were significantly linked to parasite genetic loci, providing important candidate genes for studying host molecules that recognize parasite ligands or pathogen-associated molecular patterns (PAMPs) (Wu et al, 2020)

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Summary

Introduction

The mechanisms for generating pir gene diversity are expected to be similar to those of var genes, including amino acid substitutions at specific antigen epitopes in response to immune pressure and the generation of new recombinant genes through genetic recombination as well as MMEJ mediated somatic deletion, insertion and translocation. Chabaudi through the mosquito changes gene expression of the pir multi-gene family in the erythrocytic cycle, leading to changes in parasite virulence and immune response in the mammalian hosts (Spence et al, 2013).

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