Abstract
Borrelia burgdorferi sensu lato species complex is capable of establishing persistent infections in a wide variety of species, particularly rodents. Infection is asymptomatic or mild in most reservoir host species, indicating successful co-evolution of the pathogen with its natural hosts. However, infected humans and other incidental hosts can develop Lyme disease, a serious inflammatory syndrome characterized by tissue inflammation of joints, heart, muscles, skin, and CNS. Although B. burgdorferi infection induces both innate and adaptive immune responses, they are ultimately ineffective in clearing the infection from reservoir hosts, leading to bacterial persistence. Here, we review some mechanisms by which B. burgdorferi evades the immune system of the rodent host, focusing in particular on the effects of innate immune mechanisms and recent findings suggesting that T-dependent B cell responses are subverted during infection. A better understanding of the mechanisms causing persistence in rodents may help to increase our understanding of the pathogenesis of Lyme disease and ultimately aid in the development of therapies that support effective clearance of the bacterial infection by the host’s immune system.
Highlights
Borrelia burgdorferi sensu lato is a species complex of spirochetal bacteria that infects a wide variety of mammals, birds, and reptiles
Spirochetes form persistent, nonresolving infections [7]. These infections do not cause noticeable manifestations of disease in P. leucopus or certain common laboratory strains of mice [Mus musculus] [8,9,10]. This suggests that B. burgdorferi has developed immune evasion strategies that allow it to persist in the face of a mammalian immune system
A better understanding of how B. burgdorferi persists long term in rodents would be useful for understanding public health risks and devising appropriate preventative measures in endemic areas
Summary
Borrelia burgdorferi sensu lato is a species complex of spirochetal bacteria that infects a wide variety of mammals, birds, and reptiles. These infections do not cause noticeable manifestations of disease in P. leucopus or certain common laboratory strains of mice [Mus musculus] [8,9,10] This suggests that B. burgdorferi has developed immune evasion strategies that allow it to persist in the face of a mammalian immune system. Such mechanisms may be the products of co-evolution with reservoir hosts, minimizing host disease manifestations while maximizing bacterial growth and transmission. Many ecological and evolutionary factors affect prevalence, persistence, and disease development by Borrelia infections in both vector and host These factors include population dynamics, dispersal/migration, and evolution of all three players, as well as environmental landscape and climate [4].
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