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Lyme Disease Pathogenesis. Curr Issues Mol Biol 2021;42:473-518



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Pubmed Central ID




Scopus ID

2-s2.0-85102523563 (requires institutional sign-in at Scopus site)   33 Citations


Lyme disease Borrelia are obligately parasitic, tick- transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir vertebrates primarily through the induction of inflammation. During transmission from the infected tick, the bacteria undergo significant changes in gene expression, resulting in adaptation to the mammalian environment. The organisms multiply and spread locally and induce inflammatory responses that, in humans, result in clinical signs and symptoms. Borrelia virulence involves a multiplicity of mechanisms for dissemination and colonization of multiple tissues and evasion of host immune responses. Most of the tissue damage, which is seen in non-reservoir hosts, appears to result from host inflammatory reactions, despite the low numbers of bacteria in affected sites. This host response to the Lyme disease Borrelia can cause neurologic, cardiovascular, arthritic, and dermatologic manifestations during the disseminated and persistent stages of infection. The mechanisms by which a paucity of organisms (in comparison to many other infectious diseases) can cause varied and in some cases profound inflammation and symptoms remains mysterious but are the subjects of diverse ongoing investigations. In this review, we provide an overview of virulence mechanisms and determinants for which roles have been demonstrated in vivo, primarily in mouse models of infection.

Author List

Coburn J, Garcia B, Hu LT, Jewett MW, Kraiczy P, Norris SJ, Skare J


Jenifer Coburn PhD Professor in the Medicine department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Arthropod Vectors
Disease Models, Animal
Disease Susceptibility
Gene Expression Regulation, Bacterial
Host-Pathogen Interactions
Lyme Disease
Virulence Factors