A Brucella Type IV Effector Targets the COG Tethering Complex to Remodel Host Secretory Traffic and Promote Intracellular Replication

Many intracellular pathogens exploit host secretory trafficking to support their intracellular cycle, but knowledge of these pathogenic processes is limited. The bacterium Brucella abortus uses a type IV secretion system (VirB T4SS) to generate a replication-permissive Brucella-containing vacuole (rBCV) derived from the host ER, a process that requires host early secretory trafficking. Here we show that the VirB T4SS effector BspB contributes to rBCV biogenesis and Brucella replication by interacting with the conserved oligomeric Golgi (COG) tethering complex, a major coordinator of Golgi vesicular trafficking, thus remodeling Golgi membrane traffic and redirecting Golgi-derived vesicles to the BCV. Altogether, these findings demonstrate that Brucella modulates COG-dependent trafficking via delivery of a T4SS effector to promote rBCV biogenesis and intracellular proliferation, providing mechanistic insight into how bacterial exploitation of host secretory functions promotes pathogenesis. [Display omitted] •The Brucella Type IV effector BspB promotes rBCV biogenesis and bacterial replication•BspB targets the COG complex to redirect vesicular traffic to the rBCV•COG-dependent membrane traffic is required for optimal bacterial replication How bacterial pathogens exploit host secretory functions to achieve their intracellular cycle remains poorly understood. Miller et al. show here that Brucella abortus delivers into macrophages a type IV-secretion effector that remodels Golgi-associated membrane traffic to promote biogenesis of the Brucella replicative vacuole and bacterial proliferation.