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        <rdfs:label>artificially mutated Brucella</rdfs:label>
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        <rdfs:label xml:lang="en">Hela cell - Brucella interaction</rdfs:label>
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        <rdfs:label xml:lang="en">Brucella intracellular growth</rdfs:label>
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        <rdfs:label xml:lang="en">Brucella intracellular replication</rdfs:label>
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        <rdfs:label xml:lang="en">Brucella virb10 mutant</rdfs:label>
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        <rdfs:comment xml:lang="en">MUTATION: Mutants with polar and nonpolar mutations introduced in  irB10 showed different behaviors in mice and in the HeLa cell infection assay, suggesting that virB10 per se is necessary for the correct function of this type IV secretion apparatus [Ref6540:Sieira et al., 2000].   A B. abortus virB10 mutant showed a decrease of intracellular live bacteria comparable to that of the wild-type strain until 4 h after infection, indicating that a functional VirB system is not required for the short-term survival of Brucella inside macrophages. At later time points, the number of live virB10 mutants  progressively decreased. Hence, the Brucella  virB10  strain did not replicate, but rather was killed. Although the  virB10 mutants are capable of short-term survival, they can not evade long-term degradation through fusion with lysosomes [Ref6547:Celli et al., 2003].  B abortus virB1 and virB10 mutants are unable to persist in mouse spleens after i.p. inoculation, suggest that attenuation in the animal model is due to an inability of these strains to grow intracellularly [Ref6463:Hong et al., 2000].  A B abortus virB10 mutant lost the ability to multiply in HeLa cells and was not recovered from the spleens of infected BALBc mice [Ref6538:Briones et al., 2001].  The non polar virB10 mutant was able to block the acquisition of cathepsin D, but was not able to translocate to the replication compartment [Ref6548:Boschiroli et al., 2002].  The virB10  non-polar mutants were capable of avoiding interactions with the endocytic pathway but , diverging to wild-type Brucella, were unable to reach the endoplasmic reticulum to establish their intracellular replication niche and seemed to be recycled to the cell surface [Ref6465:Comerci et al., 2001].</rdfs:comment>
        <ns3:IAO_0000232 xml:lang="en">See PMID:10940027, 12925673, 10858227, 11401996, 12414154, 11260139</ns3:IAO_0000232>
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