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      Toxoplasma gondii and the blood-brain barrier

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          Abstract

          Infection with the protozoan parasite Toxoplasma gondii is characterized by asymptomatic latent infection in the central nervous system and skeletal muscle tissue in the majority of immunocompentent individuals. Life-threatening reactivation of the infection in immunocompromized patients originates from rupture of Toxoplasma cysts in the brain. While major progress has been made in our understanding of the immunopathogenesis of infection the mechanism(s) of neuroinvasion of the parasite remains poorly understood. The present review presents the current understanding of blood-brain barrier (patho)physiology and the interaction of Toxoplasma gondii with cells of the blood-brain barrier.

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          Most cited references 131

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          Endothelial cell-cell junctions: happy together.

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            Polymorphic secreted kinases are key virulence factors in toxoplasmosis.

            The majority of known Toxoplasma gondii isolates from Europe and North America belong to three clonal lines that differ dramatically in their virulence, depending on the host. To identify the responsible genes, we mapped virulence in F(1) progeny derived from crosses between type II and type III strains, which we introduced into mice. Five virulence (VIR) loci were thus identified, and for two of these, genetic complementation showed that a predicted protein kinase (ROP18 and ROP16, respectively) is the key molecule. Both are hypervariable rhoptry proteins that are secreted into the host cell upon invasion. These results suggest that secreted kinases unique to the Apicomplexa are crucial in the host-pathogen interaction.
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              Toxoplasma gondii comprises three clonal lineages: correlation of parasite genotype with human disease.

               Laura Howe,  L. Sibley (1995)
              The population genetic structure of Toxoplasma gondii was determined by multilocus restriction fragment length polymorphism analysis at 6 loci in 106 independent isolates from humans and animals. Phylogenetic and statistical analyses indicated a highly unusual population structure consisting of 3 widespread clonal lineages. Extensively mixed genotypes were only apparent in 4 strains, which indicated that, while not separate species, sexual recombination between the 3 lineages is exceedingly rare in natural populations. T. gondii is a major cause of subclinical human infection and an important opportunistic pathogen that causes severe disease in immunocompromised patients. While strains from all 3 lineages were isolated from humans, the majority of human toxoplasmosis cases were associated with strains of a type II genotype. The correlation of specific clonal lineages with human toxoplasmosis has important implications for development of vaccines, drug treatments, and diagnostic protocols.
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                Author and article information

                Journal
                Virulence
                Virulence
                VIRU
                Virulence
                Landes Bioscience
                2150-5594
                2150-5608
                01 March 2012
                01 March 2012
                : 3
                : 2
                : 182-192
                Affiliations
                [1 ]Institute for Microbiology and Hygiene; Charité Medical School; Berlin, Germany
                [2 ]Glasgow Biomedical Research Centre; University of Glasgow; Glasgow, UK
                Author notes
                [†]

                Current affiliation: Medical and Scientific Affairs; Roche Molecular Diagnostics; Pleasanton, CA USA

                [* ]Correspondence to: Oliver Liesenfeld, Email: oliver.liesenfeld@ 123456charite.de
                Article
                2011VIRULENCE0051R 19004
                10.4161/viru.19004
                3396697
                22460645
                Copyright © 2012 Landes Bioscience

                This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

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