ABSTRACT:
India, being a developing country, incidence of malarial infection prevail as a major socio-economic problem, though the infection is both treatable and preventable. There are nine anopheline vectors to transmit three specific Plasmodial species, P. falciparum, P. vivax and P. malariae, where the parasite develops intracellularly within the altered host red blood cell. Recently, it has been identified that a membranous structure called Maurer’s Cleft (MC) is formed by P. falciparum for protein sorting and export in order to remodel the erythrocyte. The five major proteins involve are Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1), the ring-exported proteins (REX) 1 and 2, repetitive interspersed family (RIFINS), a subtelomeric variable open reading frame (STE-VORS) and Plasmodium falciparum Maurer’s clefts two transmembrane protein (PfMC-2TM). Among REX 1 is reported to persists throughout the life cycle of the parasite and also involve a novel PEXEL (a motif which possess recessed signal sequence for entering the erythrocyte) independent export pathway. Most importantly, the role of REX 1 in the maintenance of MC architecture, where the truncation of REX 1 gene in P. falciparum strain D10 results in distortion of MC morphology and decrease in the number of MC. Addition to those MC cisternae seems stacked or multilamellate. Hence, REX 1 could serve as an exclusive target to intervene the process in erythrocyte remodelling and is considered for the present study. The present study indicates the significant interaction showed by the antimalarial drugs with REX1.