: A Drive to Survive.

is an obligate intracellular protozoan parasite that causes zoonotic disease. Central to its pathogenesis is the ability of the parasite to invade host red blood cells of diverse species, and, once in the host blood stream, to manipulate the composition of its population to allow it to endure unfavorable conditions. Here we will review key in vitro studies relating to the survival strategies that adopts during its intraerythrocytic development to persist and how proliferation is restored in the parasite population once optimum conditions return.

Identification and Characterization of the Rhoptry Neck Protein 2 in Babesia divergens and B. microti.

Apicomplexan parasites include those of the genera Plasmodium, Cryptosporidium, and Toxoplasma and those of the relatively understudied zoonotic genus Babesia In humans, babesiosis, particularly transfusion-transmitted babesiosis, has been emerging as a major threat to public health. Like malaria, the disease pathology is a consequence of the parasitemia which develops through cyclical replication of Babesia parasites in host erythrocytes. However, there are no exoerythrocytic stages in Babesia, so targeting of the blood stage and associated proteins to directly prevent parasite invasion is the most desirable option for effective disease control.

A malaria vaccine candidate based on an epitope of the Plasmodium falciparum RH5 protein.

Background: The Plasmodium falciparum protein RH5 is an adhesin molecule essential for parasite invasion of erythrocytes. Recent studies show that anti-PfRH5 sera have potent invasion-inhibiting activities, supporting the idea that the PfRH5 antigen could form the basis of a vaccine. Therefore, epitopes recognized by neutralizing anti-PfRH5 antibodies could themselves be effective vaccine immunogens if presented in a sufficiently immunogenic fashion.

Babesia and red cell invasion.

Purpose Of Review: Babesiosis is a zoonosis, a disease communicable from animals to humans and an important blood-borne human parasitic infection. Despite its public health impact, its study has largely been neglected. The objective of this review is to present up-to-date information on both parasite and red blood cell molecules that function at the host-parasite interface to facilitate successful invasion.

Babesia divergens and Plasmodium falciparum use common receptors, glycophorins A and B, to invade the human red blood cell.

Babesiosis has long been recognized as an economically important disease of cattle, but only in the last 30 years has Babesia been recognized as an important pathogen in humans. Invasion of erythrocytes is an integral part of the Babesia life cycle. However, very little information is available on the molecules involved in this process, in contrast to another hemoparasite, Plasmodium falciparum.

Invasion profiles of Brazilian field isolates of Plasmodium falciparum: phenotypic and genotypic analyses.

The invasion of red blood cells (RBCs) by Plasmodium falciparum is dependent on multiple molecular interactions between erythrocyte receptors and parasite ligands. Invasion studies using culture-adapted parasite strains have indicated significant receptor heterogeneity. It is not known whether this heterogeneity reflects the parasite invasion arsenal in the field.