Host-Plasmodium interaction: role of RNAi

Malaria is a global health problem that afflicts an estimated 90 million people worldwide. Significant improvement in the understanding of Plasmodium life cycle has been achieved, yet multitude of clinical effects seen in malaria remains unanswered. MicroRNAs (miRNAs) have been implicated in the pathogenesis of malaria. These miRNAs act as post-transcriptional regulators and control host's cellular factors needed for Plasmodium multiplication and suppress immune responses. Dysregulated miRNA expression has been linked to malaria pathogenesis through modulation of signalling pathways involved in processes such as proliferation, metabolism, gene expression and immune response in the host. In humans, Plasmodium infection severely affects hepatic functions and erythrocytic life span while severe infection with P. falciparum can lead to cerebral pathology. The present review aims to gain insight into the contribution of miRNAs to the exo-erythrocytic and erythrocytic stage pathology of Plasmodium infection and coordinated regulation in Plasmodium-mediated progression to cerebral pathology.