Abstract
Malaria, a vector-borne debilitating disease, caused by the Apicomplexan parasite Plasmodium is transmitted by female Anopheles mosquitoes to human host by taking a blood meal. While there are many species that infect humans, two of which are of major public health burden: P. falciparum, accounting for ~90% global cases, causes severe form of malaria, while benign P. vivax species accounting for ~40% of South-east Asian cases. Despite its considerable impact in global public health, P. vivax was for long time a neglected parasite as represent asymptomatic condition contributing to being classically recognized as a benign infection. Red cell tropism during the asexual intraerythrocytic developmental cycle (IDC) possibly leading to molecular alterations of the parasite physiological states may be an important contributor to selective infection. The ability of P. falciparum to infect both reticulocytes and mature RBCs (normocytes) provide an avenue to investigate potential differences in the infectious cycle in two distinct types of host cells, which forms the motivation of this PhD study. We hereby provide a hitherto unavailable body of information on biochemical and biophysical uniqueness of human reticulocytes and their potential relevance to Plasmodium infectivity, tropism and drug resistance based on which novel anti-parasitic strategies could be developed.