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. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: Microbiol Spectr. 2016 Feb;4(1):10.1128/microbiolspec.VMBF-0005-2015. doi: 10.1128/microbiolspec.VMBF-0005-2015

Figure 8. Model for VlsE-mediated protection of B. burgdorferi surface antigens.

Figure 8

A) Shortly after host infection, upregulation of vlsE expression leads to surface localization of the encoded lipoprotein. Interaction of VlsE with other proteins results in a complex that functions to shield epitopes of these surface antigens. Continued vls gene conversion leading to production of VlsE variants is necessary to avoid killing by antibodies raised against the parental and subsequent VlsE variants, allowing for sustained epitope masking. Absence (panel B) or low expression (panel C) of VlsE allows binding of neutralizing antibodies to B. burgdorferi surface antigens that ultimately leads to spirochete death (denoted by a large red X). A legend indicating the identity of the various molecular cartoon depictions is provided at the bottom of the figure.