Abstract
Brucellosis is a highly prevalent zoonotic disease caused by Brucella. Brucella spp. are gram-negative facultative intracellular parasitic bacteria. Its intracellular survival and replication depend on a functional virB system, an operon encoded by VirB1–VirB12. Type IV secretion system (T4SS) encoded by the virB operon is an important virulence factor of Brucella. It can subvert cellular pathway and induce host immune response by secreting effectors, which promotes Brucella replication in host cells and induce persistent infection. Therefore, this paper summarizes the function and significance of the VirB system, focusing on the structure of the VirB system where VirB T4SS mediates biogenesis of the endoplasmic reticulum (ER)-derived replicative Brucella-containing vacuole (rBCV), the effectors of T4SS and the cellular pathways it subverts, which will help better understand the pathogenic mechanism of Brucella and provide new ideas for clinical vaccine research and development.
Highlights
Brucella can invade the body through skin mucosa, digestive tract and respiratory tract; it is enclosed in a membrane to form a Brucella-containing vacuole (BCV) [54]; subsequently, early endosomal markers (EEA-1, Rab5) and late endosomal markers (LAMP1, Rab7, CD63, RILP) are obtained [55,56,57], which decreases PH and induces expression of VirB T4SS
The expression of the VirB system peaked during replicative Brucella-containing vacuole (rBCV) biogenesis, but the bacteria gradually began to decrease when replicating in the host cell, which indicates that the expression of the VirB system is strictly regulated in the host cell [76]
The intracellular replication of Brucella relies on the formation of T4SS encoded by VirB, which regulates host cell pathways through the release of effectors
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Human disease is caused by direct contact with the blood or tissue of infected animals or by consumption of contaminated dairy products, with clinical symptoms such as intermittent fever, arthritis, orchitis, hepatitis, and depression [2,3]. Brucella causes host pathogenesis through survival and replication in target cells, an intracellular process dependent on T4SS encoded by the VirB operon [6]. When the replication niche is established, VirB T4SS is inhibited. VirB system in the intracellular circulation has been largely elucidated, there are still some deficiencies. This paper will elaborate on the mechanism of VirB action to provide a theoretical basis for the pathogenesis of Brucella and clinical vaccine development. Sci. 2021, 22, 13637a theoretical basis for the pathogenesis of Brucella and clinical vaccine development
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