Antigenic Variation of VlsE in Borrelia burgdorferi

Abstract

The multisystem disease known as Lyme disease (or Lyme borreliosis) is the most prevalent vector-borne infection affecting humans in North America and Europe (Barbour 2001; Steere et al. 2004). Causative bacterial agents of the disease, the spirochetes Borrelia burgdorferi, Borrelia garinii, and Borrelia afzelii, are transmitted by hard-bodied ticks of the genus Ixodes. Infected ticks transmit Lyme disease Borreliae to humans during feeding, which can result in a localized infection (erythema migrans) at the site of the tick bite. Disseminated and chronic stages of infection follow; these are characterized by neurological, cardiac, and arthritic manifestations of disease. Infection with Lyme disease Borrelia can last from months to years due to avoidance of the host immune response, and key to its successful evasion tactics is recombination at the vls locus located at the telomeric end of a 28-kb linear plasmid (Norris 2006; Palmer et al. 2009; Zhang et al. 1997). Recombinational switching at the vls locus results in sequence variation of the surface protein, VlsE, thus altering its antigenic properties and allowing the spirochete to evade the host’s antibody-mediated response (Zhang et al. 1997; Zhang and Norris 1998a, b).