Pathogenicity and virulence of Brucella: Strategies for metabolic adaptation and immune evasion

Brucella species are facultative intracellular pathogens that have evolved sophisticated mechanisms to evade host immune responses and establish chronic infections. This review provides an analysis of Brucella virulence and pathogenicity, with particular emphasis on the intricate interactions between the pathogen and its host. We examine the molecular and cellular mechanisms underlying Brucella pathogenesis, detailing the processes by which the bacterium invades, survives, and replicates within host cells. An in-depth discussion of the key Brucella virulence factors and their roles in immune evasion is provided, including strategies that enable the pathogen to circumvent immune detection, subvert host immune signaling pathways, and manipulate intracellular trafficking. Furthermore, we explore Brucella ability to modulate host cellular functions, particularly through the induction of the unfolded protein response and its implications for bacterial persistence. The review also highlights the influence of type I interferon responses on host susceptibility to Brucella infection, shedding light on their role in disease progression. Additionally, we discuss Brucella metabolic adaptations, including its ability to exploit host-derived nutrients and reprogram metabolic pathways to sustain long-term persistence. Finally, we address emerging research directions and future perspectives in the field, emphasizing the need for novel therapeutic and vaccine strategies. A deeper understanding of these complex host-pathogen interactions will be instrumental in developing more effective approaches for the control, prevention, and treatment of brucellosis.