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dc.contributor.authorKappmeyer, Lowell Sen_US
dc.contributor.authorThiagarajan, Mathangien_US
dc.contributor.authorHerndon, David Ren_US
dc.contributor.authorRamsay, Joshua Den_US
dc.contributor.authorCaler, Elisabeten_US
dc.contributor.authorDjikeng, Appolinaireen_US
dc.contributor.authorGillespie, Joseph Jen_US
dc.contributor.authorLau, Audrey OTen_US
dc.contributor.authorRoalson, Eric Hen_US
dc.contributor.authorSilva, Joana Cen_US
dc.contributor.authorSilva, Marta Gen_US
dc.contributor.authorSuarez, Carlos Een_US
dc.contributor.authorUeti, Massaro Wen_US
dc.contributor.authorNene, Vishvanath Men_US
dc.contributor.authorMealey, Robert Hen_US
dc.contributor.authorKnowles, Donald Pen_US
dc.contributor.authorBrayton, Kelly Aen_US
dc.identifier.citationBMC Genomics. 2012 Nov 09;13(1):603en_US
dc.description.abstractAbstract Background Transmission of arthropod-borne apicomplexan parasites that cause disease and result in death or persistent infection represents a major challenge to global human and animal health. First described in 1901 as Piroplasma equi, this re-emergent apicomplexan parasite was renamed Babesia equi and subsequently Theileria equi, reflecting an uncertain taxonomy. Understanding mechanisms by which apicomplexan parasites evade immune or chemotherapeutic elimination is required for development of effective vaccines or chemotherapeutics. The continued risk of transmission of T. equi from clinically silent, persistently infected equids impedes the goal of returning the U. S. to non-endemic status. Therefore comparative genomic analysis of T. equi was undertaken to: 1) identify genes contributing to immune evasion and persistence in equid hosts, 2) identify genes involved in PBMC infection biology and 3) define the phylogenetic position of T. equi relative to sequenced apicomplexan parasites. Results The known immunodominant proteins, EMA1, 2 and 3 were discovered to belong to a ten member gene family with a mean amino acid identity, in pairwise comparisons, of 39%. Importantly, the amino acid diversity of EMAs is distributed throughout the length of the proteins. Eight of the EMA genes were simultaneously transcribed. As the agents that cause bovine theileriosis infect and transform host cell PBMCs, we confirmed that T. equi infects equine PBMCs, however, there is no evidence of host cell transformation. Indeed, a number of genes identified as potential manipulators of the host cell phenotype are absent from the T. equi genome. Comparative genomic analysis of T. equi revealed the phylogenetic positioning relative to seven apicomplexan parasites using deduced amino acid sequences from 150 genes placed it as a sister taxon to Theileria spp. Conclusions The EMA family does not fit the paradigm for classical antigenic variation, and we propose a novel model describing the role of the EMA family in persistence. T. equi has lost the putative genes for host cell transformation, or the genes were acquired by T. parva and T. annulata after divergence from T. equi. Our analysis identified 50 genes that will be useful for definitive phylogenetic classification of T. equi and closely related organisms.en_US
dc.rightsAttribution 4.0 United States*
dc.titleComparative genomic analysis and phylogenetic position of Theileria equien_US
dc.typeJournal articleen_US
dc.description.versionPeer Revieweden_US
dc.rights.holderLowell S Kappmeyer et al.; licensee BioMed Central Ltd.en_US

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