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Borrelia burgdorferi , the pathogen of Lyme disease, cycles in nature through  Ixodes  ticks and mammalian hosts. At least five Complement Regulator-Acquiring Surface Proteins (BbCRASPs) are produced by  B. burgdorferi , which are thought to assist spirochetes in host immune evasion. Recent studies established that BbCRASP-2 is preferentially expressed in mammals, and elicits robust antibody response in infected hosts, including humans. We show that  BbCRASP-2  is ubiquitously expressed in diverse murine tissues, but not in ticks, reinforcing a role of BbCRASP-2 in conferring  B. burgdorferi  defense against persistent host immune threats, such as complement. BbCRASP-2 immunization, however, fails to protect mice from  B. burgdorferi  infection and does not modify disease, as reflected by the development of arthritis. An infectious  BbCRASP-2  mutant was generated, therefore, to examine the precise role of the gene product in spirochete infectivity. Similar to wild type  B. burgdorferi, BbCRASP-2  mutants remain insensitive to complement-mediated killing  in vitro , retain full murine infectivity and induce arthritis. Quantitative RT-PCR assessment indicates that survivability of BbCRASP-2-deficient  B. burgdorferi  is not due to altered expression of other  BbCRASP s. Together, these results suggest that the function of a selectively expressed  B. burgdorferi  gene,  BbCRASP-2 , is not essential for complement resistance or infectivity in the murine host.

Borrelia burgdorferi Complement Regulator-Acquiring Surface Protein 2 Does Not Contribute to Complement Resistance or Host Infectivity