Role of VIsE in host reinfection by the lyme disease spirochete, borretia burgdorferi
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A key mechanism for immune evasion and persistent infection by the causative agent of Lyme borreliosis, Borrelia burgdorferi (Bb), is antigenic variation of the immunodominant VIsE surface protein. Although a multitude of other surface proteins exist that are immunogenic, VIsE is the only know Bb antigen that exhibits variation of its surface epitopes. A long-standing question regarding Bb immune escape has been how such a feat is accomplished through sequence variation of this single lipoprotein, despite the presence of a substantial number of additional antigens residing on the bacterial surface. In other bacterial pathogen systems, the dominant presence of surface-exposed variable proteins had been associated with the ability to reinfect a host. In the current study, we investigated whether host reinfection by Bb requires VIsE, and the likely mechanism involved. Host-adapted wild-type and VIsE mutant spirochetes were used to reinfect immunocompetent mice that had naturally cleared an infection with a VIsE-deficient clone. Our results demonstrated that VIsE is necessary for reinfection by Bb, and this ability is directly related to evasion of the host antibody response. Moreover, the data presented here raise the possibility that escape of Bb surface antigens from immune surveillance may involve epitope shielding by the VIsE protein.