Year: 2020
Type: article
Abstract: Babesia bovis causes a pathogenic form of babesiosis in cattle.Following invasion of red blood cells (RBCs) the parasite extensively modifies host cell structural and mechanical properties via the export of numerous proteins.Despite their crucial role in virulence and pathogenesis, such proteins have not been comprehensively characterized in B. bovis.Here we describe the surface biotinylation of infected RBCs (iRBCs), followed by proteomic analysis.We describe a multigene family (mtm) that encodes predicted multi-transmembrane integral membrane proteins which are exported and expressed on the surface of iRBCs.One mtm gene was downregulated in blasticidin-S (BS) resistant parasites, suggesting an association with BS uptake.Induced knockdown of a novel exported protein encoded by BBOV_III004280, named VESA export-associated protein (BbVEAP), resulted in a decreased growth rate, reduced RBC surface ridge numbers, mis-localized VESA1, and abrogated cytoadhesion to endothelial cells, suggesting that BbVEAP is a novel virulence factor for B. bovis. Author summaryBabesia bovis is an apicomplexan intraerythrocytic protozoan parasite which causes the most pathogenic form of babesiosis in cattle.Like other apicomplexan parasites, B. bovisinduced modification of host cells is crucial for its survival.However, our knowledge of Babesia surface exposed proteins is limited to variant erythrocyte surface antigen1 (VESA1), which is responsible for fatal cerebral babesiosis.Here we identified two novel exported proteins in B. bovis using red blood cell (RBC) surface biotinylation and mass spectrometry.One of the proteins was determined to be essential for parasite development and pathogenicity.Induced knockdown of this protein resulted in a decreased growth rate, reduced RBC surface protrusions created by the parasite, mis-localized VESA1, and
Source: PLoS Pathogens
Institutions: Nagasaki University, National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Institute of Tropical Medicine, Nagasaki University, Hokkaido University, Hokkaido University International Institute for Zoonosis Control, Nagoya University
Language: English
Subfield: Parasitology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,500
Awards: Study on glidinig motility of Babesia bovis merozoite, Elucidation of Plasmodium knowlesi molecules involved in human endothelial cell adhesion, 脳性バベシア症における原虫感染赤血球接着機構の解明, Studies on development of the Babesia parasites that express cytokine for non-specific immune activation, High-speed AFM study on functional modulation of kinesin caused by structural defects of mictoruble, G4483555629, Comprehensive analysis of Babesia tick-stage antigens: Establishing of a base for development the TBV, Gliding motility in malaria parasites during erythrocyte invasion, G6444557475, Molecular mechanisms of gliding motility and erythrocyte invasion by Plasmodium falciparum, Study on cytoadhesion mechanism of Babesia bovis-infected erythrocytes, G740839079, G743007687, Identification and Functional Characterization of Babesia bovis Exportome, Functional characterization of Babesia bovis proteins expressed on the surface of infected erythrocytes- Toward identification of novel vaccine and therapeutic candidates, Merozoite gliding motility and erythrocyte invasion by malaria parasite(Fostering Joint International Research)
OpenAlex ID: W3089873386