Abstract
Bovine babesiosis is an acute and persistent tick-borne global disease caused mainly by the intraerythrocytic apicomplexan parasites Babesia bovis and B. bigemina. B. bovis infected erythrocytes sequester in blood capillaries of the host (cytoadhesion), causing malaria-like neurological signs. Cytoadhesion and antigenic variation in B. bovis are linked to the expression of members of the Variant Erythrocyte Surface Antigen (VESA) gene family. Animals that survive acute B. bovis infection and those vaccinated with attenuated strains remain persistently infected, suggesting that B. bovis parasites use immune escape mechanisms. However, attenuated B. bovis parasites do not cause neurological signs in vaccinated animals, indicating that virulence or attenuation factors play roles in modulating parasite virulence phenotypes. Artificial overexpression of the SBP2t11 protein, a defined attenuation factor, was associated with reduced cytoadhesion, suggesting a role for this protein as a key modulator of virulence in the parasite. Hereby, we propose a model that might be functional in the modulation of B. bovis virulence and persistence that relies on the interplay among SBP2t, VESA proteins, cytoadhesion, and the immune responses of the host. Elucidation of mechanisms used by the parasite to establish persistent infection will likely contribute to the design of new methods for the control of bovine babesiosis.
Highlights
Apicomplexa is a phylum of obligatory parasitic protozoans that are comprised of the obligate endoparasites of animals and humans, which share complex apical structures in their zoite stages and are specialized for cell attachment and invasion [1]
It is reasonable to speculate that the B. bovis Variant Erythrocyte Surface Antigen (VESA) and SBP2 proteins have similar characteristics and roles as PfEMP1 and knob-associated histidine-rich protein (KAHRP) in P. falciparum, respectively
VESA proteins have been involved in cytoadhesion and have undergone antigenic variation encoded by the ves multigene family
Summary
Apicomplexa is a phylum of obligatory parasitic protozoans that are comprised of the obligate endoparasites of animals and humans, which share complex apical structures in their zoite stages and are specialized for cell attachment and invasion [1]. The complement of secretory organelles contains proteins needed for cell invasion, a critical parasite function that usually causes pathological consequences for the host, and at least some apical complex molecules could as virulence factors. Babesia are causes pathological consequences for the host, and thusbe atconsidered least some apical complex molecules could tick-borne apicomplexan that are the causative agents of parasites babesiosis: most be considered as virulenceparasites factors. Babesia are tick-borne apicomplexan thatone are of thethe causative common arthropod-borne infections of free-living animals worldwide [4]. More than 100 species of Babesia can infect numerous tick vectors and mammalian bigemina (the causative agents bovis of bovine have a large impact on thebabesiosis) beef and have dairya hosts, and among them, Babesia and B.babesiosis) bigemina Cryptosporidium have mitochondria in size and known function as a mitosome
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