bearer of at some time only_in_taxon Brucella virulence factor disposition Brucella melitensis bv. 1 str. 16M BMEII0025 protein attachment mediating protein VIRB1-like protein This protein is a Brucella virulence factor. MUTATION: The Brucella abortus virB operon, encoding a type IV secretion system (T4SS), is required for intracellular replication and persistent infection in the mouse model. The products of the first two genes of the virB operon, virB1 and virB2, are predicted to be localized at the bacterial surface. Both mutants were shown to be nonpolar, as demonstrated by their ability to express the downstream gene virB5 during stationary phase of growth in vitro. Both VirB1 and VirB2 were essential for intracellular replication in J774 macrophages. The nonpolar virB1 mutant persisted at wild-type levels, showing that the function of VirB1 is dispensable in the mouse model of persistent infection [Ref6539:den et al., 2004]. A B abortus polar virB1 mutant failed to replicate in HeLa cells, indicating that the virB operon plays a critical role in intracellular multiplication [Ref6540:Sieira et al., 2000]. Polar mutations in the virB1 to virB2 intergenic region or in virB2 reduced the detection of VirB5 to a greater extent than they did that of VirB12. A virB1 mutation also eliminates the transcription of virB12 in B suis [Ref6470:Sun et al., 2005]. An infection assay with signature-tagged Brucella abortus mutants demonstrated that mutagenesis of the virB1 gene causes attenuation of virulence [Ref6471:Höppner et al., 2005]. NCBIGene: 1197796 NCBIProteinAccess:NP_541002 GenBank: AE008918 LocusTag: BMEII0025 PMID: 15322008, 10940027, 16113325, 16272371 NCBIProteinGI: 17988369 Molecule Role Annotation: MUTATION: The Brucella abortus virB operon, encoding a type IV secretion system (T4SS), is required for intracellular replication and persistent infection in the mouse model. The products of the first two genes of the virB operon, virB1 and virB2, are predicted to be localized at the bacterial surface. Both mutants were shown to be nonpolar, as demonstrated by their ability to express the downstream gene virB5 during stationary phase of growth in vitro. Both VirB1 and VirB2 were essential for intracellular replication in J774 macrophages. The nonpolar virB1 mutant persisted at wild-type levels, showing that the function of VirB1 is dispensable in the mouse model of persistent infection [Ref6539:den et al., 2004]. A B abortus polar virB1 mutant failed to replicate in HeLa cells, indicating that the virB operon plays a critical role in intracellular multiplication [Ref6540:Sieira et al., 2000]. Polar mutations in the virB1 to virB2 intergenic region or in virB2 reduced the detection of VirB5 to a greater extent than they did that of VirB12. A virB1 mutation also eliminates the transcription of virB12 in B suis [Ref6470:Sun et al., 2005]. An infection assay with signature-tagged Brucella abortus mutants demonstrated that mutagenesis of the virB1 gene causes attenuation of virulence [Ref6471:Höppner et al., 2005]. Gene name: virb1 UniProtKB: PR:Q8YDZ5