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The primary causative agent of tick-borne relapsing fever in North America isBorrelia hermsii . It has been hypothesized thatB. hermsii evades complement-mediated destruction by binding factor H (FH), a host-derived negative regulator of complement.In vitro ,B. hermsii produces a single FH binding protein designated FhbA (FH binding protein A). The properties and ligand binding activity of FhbA suggest that it plays multiple roles in pathogenesis. It binds plasminogen and has been identified as a significant target of a B1b B cell-mediated IgM response in mice. FhbA has also been explored as a potential diagnostic antigen forB. hermsii infection in humans. The ability to test the hypothesis that FhbA is a critical virulence factorin vivo has been hampered by the lack of well-developed systems for the genetic manipulation of the relapsing fever spirochetes. In this report, we have successfully generated aB. hermsii fhbA deletion mutant (theB. hermsii YORΔfhbA strain) through allelic exchange mutagenesis. Deletion offhbA abolished FH binding by the YORΔfhbA strain and eliminated cleavage of C3b on the cell surface. However, the YORΔfhbA strain remained infectious in mice and retained resistance to killingin vitro by human complement. Collectively, these results indicate thatB. hermsii employs an FhbA/FH-independent mechanism of complement evasion that allows for resistance to killing by human complement and persistence in mice.

The Borrelia hermsii Factor H Binding Protein FhbA Is Not Required for Infectivity in Mice or for Resistance to Human Complement In Vitro