NIH R01 · 2025
Summary The ability of Borrelia burgdorferi to cause Lyme disease is highly dependent on its capacity to establish a successful infection upon entering the mammalian host. Moreover, survival of the pathogen in nature is completely dependent on its enzootic life cycle involving both a tick and reservoir host. The transition between these two very different host types requires the ability to rapidly adapt through changes in gene expression. Recent studies in our lab have provided evidence of the importance of lp17-resident genes for plasmid copy number control and resultant gene dosage effects that may have significant roles in host adaptation by B. burgdorferi. Despite this advance, there…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.