Interplay between attenuation-and virulence-factors of Babesia bovis and their contribution to the establishment of persistent infections in cattle

Authors: GALLEGO-LÓPEZ, GINA - Washington State University; COOKE, B - Washington State University; Suarez, Carlos

Submitted to: Pathogens
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/29/2019
Publication Date: 7/4/2019
Citation: Gallego-López, G.M., Cooke, B.M., Suarez, C.E. 2019. Interplay between attenuation-and virulence-factors of Babesia bovis and their contribution to the establishment of persistent infections in cattle. Pathogens. 8(3). https://doi.org/10.3390/pathogens8030097.
DOI: https://doi.org/10.3390/pathogens8030097

Interpretive Summary: Bovine babesiosis is an acute and persistent costly tick-borne global disease caused mainly by Babesia bovis and B. bigemina. B. bovis sequesters in blood capillaries of the host, causing malaria-like neurological signs. Animals that survive acute B. bovis infection remain persistently infected suggesting that B. bovis uses successful immune escape mechanisms. Attenuated B. bovis parasites can also cause mild acute and persistent disease without causing neurological signs in vaccinated animals, suggesting that virulence or attenuation factors may play roles in modulating parasite virulence phenotypes. Hereby we propose a model to explain current data the interplay among parasite proteins, cythoadhesion and the immune responses of the host. In the modulation of B. bovis virulence and persistence elucidation of mechanisms used by the parasite to establish persistent infection will surely contribute to the design of new methods for the control of bovine babesiosis.

Technical Abstract: Bovine babesiosis is an acute and persistent costly tick-borne global disease caused mainly by Babesia bovis and B. bigemina. B. bovis sequesters in blood capillaries of the host, causing malaria-like neurological signs. Capillary sequestration 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 remain persistently infected suggesting that B. bovis use successful immune escape mechanisms. Attenuated B. bovis parasites can also cause mild acute and persistent disease without causing neurological signs in vaccinated animals, suggesting that virulence or attenuation factors may play roles in modulating parasite virulence phenotypes. Artificial overexpression of the SBP2t11 protein, a previously 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, cythoadhesion and the immune responses of the host. Elucidation of mechanisms used by the parasite to establish persistent infection will surely contribute to the design of new methods for the control of bovine babesiosis.