bearer of at some time only_in_taxon Brucella virulence factor disposition Brucella melitensis bv. 1 str. 16M BMEII0034 protein channel protein VIRB10-like protein UniProtKB: PR:Q8YDZ0 Gene name: virb10 NCBIProteinAccess:NP_541011 LocusTag: BMEII0034 This protein is a Brucella virulence factor. 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]. Molecule Role Annotation: 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]. GenBank: AE008918 PMID: 10940027, 12925673, 10858227, 11401996, 12414154, 11260139 NCBIProteinGI: 17988378 NCBIGene: 1197805