Abstract
Brucella spp. are intracellular bacterial pathogens that cause infection in domestic and wild animals. They are often used as model organisms to study intracellular bacterial infections. Brucella VirB T4SS is a key virulence factor that plays important roles in mediating intracellular survival and manipulating host immune response to infection. In this review, we discuss the roles of Brucella VirB T4SS and 15 effectors that are proposed to be crucial for Brucella pathogenesis. VirB T4SS regulates the inflammation response and manipulates vesicle trafficking inside host cells. VirB T4SS also plays crucial roles in the inhibition of the host immune response and intracellular survival during infection. Here, we list the key molecular events in the intracellular life cycle of Brucella that are potentially targeted by the VirB T4SS effectors. Elucidating the functions of these effectors will help clarify the molecular role of T4SS during infection. Furthermore, studying the effectors secreted by Brucella spp. might provide insights into the mechanisms used by the bacteria to hijack the host signaling pathways and aid in the development of better vaccines and therapies against brucellosis.
Highlights
Brucella spp. cause brucellosis in domestic and wild animals
The results indicate that T4SS plays crucial roles in the inhibition of the host innate immune response and in intracellular survival during infection
The results revealed that T4SS-deficient Brucella still invaded host cells and interacted with the early and late endosomes in a manner similar to that by wild-type bacteria, as suggested by the acquisition of the early and late endosome markers (EEA1 and LAMP1, respectively) by the Brucella-containing vacuole” (BCV) (Delrue et al, 2001; Celli et al, 2003)
Summary
Brucella spp. cause brucellosis in domestic and wild animals. Their primary hosts include sheep, cattle, swine, dogs, camels, and desert woodrats (Martirosyan et al, 2011; Bargen et al, 2012).
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