Relapsing Fever SpirochetesBorrelia recurrentisandB. duttoniiAcquire Complement Regulators C4b-Binding Protein and Factor H

• DOI: 10.1128/iai.00007-06
• Publication Date: 2006-06-21T23:10:29Z
• Authors: T. Meri; S. J. Cutler; A. M. Blom; S. Meri; T. S. Jokiranta
• Keywords: 0303 health sciences; 03 medical and health sciences; Complement Inactivating Agents; Borrelia; Borrelia burgdorferi; Complement C4b-Binding Protein; Complement Factor H; Relapsing Fever; Humans; 3. Good health

ABSTRACTRelapsing fever is a rapidly progressive and severe septic disease caused by certainBorreliaspirochetes. The disease is divided into two forms, i.e., epidemic relapsing fever, caused byBorrelia recurrentisand transmitted by lice, and the endemic form, caused by severalBorreliaspecies, such asB. duttonii, and transmitted by soft-bodied ticks. The spirochetes enter the bloodstream by the vector bite and live persistently in plasma even after the development of specific antibodies. This leads to fever relapses and high mortality and clearly indicates that theBorreliaorganisms utilize effective immune evasion strategies. In this study, we show that the epidemic relapsing fever pathogenB. recurrentisand an endemic relapsing fever pathogen,B. duttonii, are serum resistant, i.e., resistant to complement in vitro. They acquire the host alternative complement pathway regulator factor H on their surfaces in a similar way to that of the less serum-resistant Lyme disease pathogen,B. burgdorferisensu stricto. More importantly, the relapsing fever spirochetes specifically bind host C4b-binding protein, a major regulator of the antibody-mediated classical complement pathway. Both complement regulators retained their functional activities when bound to the surfaces of the spirochetes. In conclusion, this is the first report of complement evasion byBorrelia recurrentisandB. duttoniiand the first report showing capture of C4b-binding protein by spirochetes.