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PLoS One 2010,5(10):e13482.PubMedCrossRef Authors’ contributions AB participated in the design of the study, performed part of the AT assays, performed MLST experiments, analysed AT and MLST data and drafted the manuscript. GS participated in the design of the study, performed part of the PFGE assays, analyzed PFGE data, performed statistical analyses and drafted the manuscript. MK maintained the strain collection and carried out part of the PFGE C646 and AT experiments. OJ conceived the study, participated in its design and coordination and revised the manuscript. NC performed AT-profile evaluation. LW participated P505-15 in vitro to AT-profile evaluation and interpretation, and critically contributed to the revision of the manuscript. All authors read and approved the final manuscript.”
“Background The eukaryotic parasite Entamoeba histolytica,

the causative agent of amebiasis, is a major cause of morbidity and mortality worldwide, as well as a category B priority biodefense pathogen [1]. In Dhaka, Bangladesh, buy NVP-BSK805 surveys done in a cohort of children living in an urban slum showed evidence of E. histolytica infection (determined by detection of parasite antigen in either diarrhea or monthly surveillance stool) in 80% of the children tested [2]. Host genetics can influence susceptibility to infectious disease and a single amino acid substitution in the host

cytokine receptor homology domain 1 of LEPR and a difference in the leukocyte antigen class II allele expressed are associated with increased susceptibility MYO10 to intestinal infection by the E. histolytica [3, 4]. Symptomatic disease occurs in only a minority of E. histolytica infections (20%) in an unpredictable manner and an initially asymptomatic infection can over time convert to invasive disease (~12.5%), amebic liver abscess can occur years after travel to an endemic area [5, 6]. It is hypothesized that both host and parasite factors contribute to the outcome of an E. histolytica[7]. However, although progress has been made in both the identification and characterization of parasite virulence factors and in understanding the regulation of their gene expression, direct manipulation of the E. histolytica genome remains elusive, and the traits affecting parasite virulence have not been genetically mapped [8–17]. Despite this variations that occur within repeat-containing genes in the amoeba genome chitinase and serine-rich E. histolytica protein SREHP have been used to examine the link between E. histolytica genetics and disease [18–22].