Borrelia burgdorferi lacking all cp32 prophage plasmids retains full infectivity in mice.

The causative agent of Lyme disease, Borrelia burgdorferi, contains a unique, segmented genome comprising multiple linear and circular plasmids. To date, the genomes of over 63 sequenced Lyme disease Borrelia carry one or more 32 kbp circular plasmids (cp32) or cp32-like elements. The cp32 plasmids are endogenous prophages and encode, among other elements, a family of surface exposed lipoproteins termed OspEF-related proteins. These lipoproteins are synthesized during mammalian infection and are considered important components of the spirochete's adaptive response to the vertebrate host. Here, we detail the construction and infectivity of the first described B. burgdorferi strain lacking all cp32 plasmids. Despite their universal presence, our findings indicate that B. burgdorferi does not require any cp32 plasmids to complete the experimental mouse-tick-mouse infectious cycle and a total lack of cp32s does not impair spirochete infectivity.