Chloroquine (CQ)-resistant Plasmodium vivax malaria was first reported 12 years ago, nearly 30 years after the recognition of CQ-resistant P. falciparum. Loss of CQ efficacy now poses a severe problem for the prevention and treatment of both diseases. Mutations in a digestive vacuole protein encoded by a 13-exon gene, pfcrt, were shown recently to have a central role in the CQ resistance (CQR) ...

Plasmodium falciparum invasion of host erythrocytes is essential for the propagation of the blood stage of malaria infection. Additionally, the brief extracellular merozoite stage of P. falciparum represents one of the rare windows during which the parasite is directly exposed to the host immune response. Therefore, efficient invasion of the host erythrocyte is necessary not only for productive...

Plasmodium falciparum malaria merozoites require erythrocyte sialic acid for optimal invasion of human erythrocytes. Since mouse erythrocytes have the form of sialic acid found on human erythrocytes (N-acetyl neuraminic acid), mouse erythrocytes were tested for invasion in vitro. The Camp and 7G8 strains of P. falciparum invaded mouse erythrocytes at 17-45% of the invasion rate of human erythro...

Malaria in pregnancy is associated with placental accumulation of Plasmodium falciparum-infected erythrocytes (IE) that adhere to chondroitin sulfate A (CSA). Adhesion is mediated by P. falciparum erythrocyte membrane protein 1 (PfEMP1), a variant parasite protein expressed on the surface of IE and encoded by var genes. Rabbit antiserum was generated against the CSA-adherent P. falciparum line ...

Malaria is an infectious disease caused by the genus Plasmodium such as Plasmodium falciparum (P. falciparum), Plasmodium ovale, Plasmodium vivax and Plasmodium malariae. Among them, P. falciparum is the parasite responsible for most severe diseases and fatal cases, which may kill over one millions of people per annum. The parasite, P. falciparum is genetically diverse and has multiple independ...

Malaria is caused by obligate intracellular parasites, of which Plasmodium falciparum is the most lethal species. In humans, P.  falciparum merozoites (invasive forms of the parasite) employ a host of parasite proteins to rapidly invade erythrocytes. One of these is the P.  falciparum apical membrane antigen 1 (PfAMA1) which forms a complex with rhoptry neck proteins at the tight junction. Here...

Polyclonal antisera raised against Plasmodium knowlesi reacted with NADP-specific glutamate dehydrogenase (GLDH) of P. knowlesi, GLDH of P. falciparum and GLDH of Proteus spp. The antisera did not react with NAD(P) GLDH from bovine liver. Polyclonal antisera raised against the GLDH of Proteus spp. cross-reacted with GLDH from P. falciparum. Monoclonal antibodies (McAbs) obtained from mice immun...

Plasmodium falciparum parasites have been endemic to Haiti for >40 years without evidence of chloroquine (CQ) resistance. In 2006 and 2007, we obtained blood smears for rapid diagnostic tests (RDTs) and filter paper blots of blood from 821 persons by passive and active case detection. P. falciparum infections diagnosed for 79 persons by blood smear or RDT were confirmed by PCR for the small sub...

Asexual stage Plasmodium falciparum replicates and undergoes a tightly regulated developmental process in human erythrocytes. One mechanism involved in the regulation of this process is posttranslational modification (PTM) of parasite proteins. Palmitoylation is a PTM in which cysteine residues undergo a reversible lipid modification, which can regulate target proteins in diverse ways. Using co...

The mechanism of switching to sexual differentiation (gametocytogenesis) of Plasmodium falciparum appears to be controlled by stochastic mechanisms that are sensitive to environmental conditions. In any given conditions, only a proportion of genetically identical parasites will become committed to sexual development. We used an experimental co-culture system to detect the presence of diffusible...