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Background  Loss of virulence is a phenotypic adaptation commonly seen in prokaryotic and eukaryotic pathogens. This mechanism is not well studied, especially in organisms with multiple host and life cycle stages such as  Babesia,  a tick-transmitted hemoparasite of humans and animals.  B. bovis,  which infects cattle, has naturally occurring virulent strains that can be reliably attenuated  in vivo . Previous studies suggest the virulence loss mechanism may involve post-genomic modification. We investigated the transcriptome profiles of two geographically distinct  B. bovis  virulent and attenuated strain pairs to better understand virulence loss and to gain insight into pathogen adaptation strategies.    Results  Expression microarray and RNA-sequencing approaches were employed to compare transcriptome profiles of two  B. bovis  strain pairs, with each pair consisting of a virulent parental and its attenuated derivative strain. Differentially regulated transcripts were identified within each strain pair. These included genes encoding for VESA1, SmORFs, undefined membrane and hypothetical proteins. The majority of individual specific gene transcripts differentially regulated within a strain were not shared between the two strains. There was a disproportionately greater number of  ves  genes upregulated in the virulent parental strains. When compared with their attenuated derivatives, divergently oriented  ves  genes were included among the upregulated  ves  genes in the virulent strains, while none of the upregulated  ves  genes in the attenuated derivatives were oriented head to head. One gene family whose specific members were consistently and significantly upregulated in expression in both attenuated strains was spherical body protein (SBP) 2 encoding gene where SBP2 truncated copies 7, 9 and 11 transcripts were all upregulated.    Conclusions  We conclude that  ves  heterodimer pair upregulation and overall higher frequency of  ves  gene expressions in the virulent strains is consistent with the involvement of this gene family in virulence. This is logical given the role of VESA1 proteins in cytoadherence of infected cells to endothelial cells. However, upregulation of some  ves  genes in the attenuated derivatives suggests that the consequence of upregulation is gene-specific. Furthermore, upregulation of the spherical body protein 2 gene family may play a role in the attenuated phenotype. Exactly how these two gene families may contribute to the loss or gain of virulence is discussed.

bmc genomics

Comparative transcriptome analysis of geographically distinct virulent and attenuated Babesia bovis strains reveals similar gene expression changes through attenuation