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dc.contributor.author Kappmeyer, Lowell S
dc.contributor.author Thiagarajan, Mathangi
dc.contributor.author Herndon, David R
dc.contributor.author Ramsay, Joshua D
dc.contributor.author Caler, Elisabet
dc.contributor.author Djikeng, Appolinaire
dc.contributor.author Gillespie, Joseph J
dc.contributor.author Lau, Audrey OT
dc.contributor.author Roalson, Eric H
dc.contributor.author Silva, Joana C
dc.contributor.author Silva, Marta G
dc.contributor.author Suarez, Carlos E
dc.contributor.author Ueti, Massaro W
dc.contributor.author Nene, Vishvanath M
dc.contributor.author Mealey, Robert H
dc.contributor.author Knowles, Donald P
dc.contributor.author Brayton, Kelly A
dc.date.accessioned 2012-11-26T13:44:40Z
dc.date.available 2012-11-26T13:44:40Z
dc.date.issued 2012-11-09
dc.identifier.citation BMC Genomics. 2012 Nov 09;13(1):603
dc.identifier.uri http://dx.doi.org/10.1186/1471-2164-13-603
dc.identifier.uri http://hdl.handle.net/10919/19074
dc.description.abstract Abstract 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.
dc.title Comparative genomic analysis and phylogenetic position of Theileria equi
dc.type Journal Article
dc.date.updated 2012-11-26T13:44:41Z
dc.description.version Peer Reviewed
dc.language.rfc3066 en
dc.rights.holder Lowell S Kappmeyer et al.; licensee BioMed Central Ltd.

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