| The Brucella abortus virB locus contains 12 open reading frames, termed virB1 through virB12, which encode a type IV secretion system (T4SS). Polar mutations in the virB locus markedly reduce the ability of B. abortus to survive in cultured macrophages or to persist in organs of mice. However they don't allow for conclusions to be drawn on the role of single genes. Here we investigated the role of each gene in the virB locus during macrophage survival and mouse virulence. Mutants carrying non-polar deletions of each gene were constructed and characterized. All mutations reduced the ability of B. abortus to survive in J774A.1 mouse macrophage-like cells to a degree similar to that caused by a deletion of the entire virB locus. Deletion of virB2, virB3, virB4, virB5, virB6, virB8, virB9, virB10 or virB11 markedly reduced the ability of B. abortus to persist in the spleens of mice at eight weeks after infection. Interestingly, deletions of virB1 and virB7 did not reduce the ability of B. abortus to persist in spleens of mice. We conclude that virB2, virB3, virB4, virB5, virB6, virB8, virB9, virB10 or virB11 are essential for mouse virulence of B. abortus while functions encoded by the virB1 and virB7 genes are not required for organ persistence in this animal model. |
