The etiologic agent of Lyme disease, Borrelia burgdorferi, is capable of circumventing the
immune defense of a variety of potential vertebrate hosts. Previous work has shown that
interaction of host-derived complement regulators, factor H and factor H-like protein 1 (FHL-
1), with up to five complement regulator-acquiring surface proteins (CRASPs) expressed by
resistant B. burgdorferi sensu lato isolates conferred complement resistance. In addition
expression of CRASP-1 is directly correlated with complement resistance of Borrelia …