RESUMO
Brucella is a broad-range, facultative intracellular pathogen that can survive and replicate in an endoplasmic reticulum (ER)-derived replication niche by preventing fusion of its membrane-bound compartment with late endosomes and lysosomes. This vacuolar hijacking was demonstrated to be dependent on the type IV secretion system VirB but no secreted effectors have been identified yet. A virB mutant is unable to reach its ER-derived replicative niche and does not multiply intracellularly. In this paper, we showed that, by co-infecting bovine macrophages or HeLa cells with the wild type (WT) strain of Brucella melitensis 16M and a deletion mutant of the complete virB operon, the replication of DeltavirB is rescued in almost 20% of the co-infected cells. Furthermore, we demonstrated that co-infections with the WT strains of Brucella abortus or Brucella suis were equally able to rescue the replication of the B. melitensis DeltavirB mutant. By contrast, no rescue was observed when the WT strain was given 1h before or after the infection with the DeltavirB mutant. Finally, vacuoles containing the rescued DeltavirB mutant were shown to exclude the LAMP-1 marker in a way similar to the WT containing vacuoles.
