Lyme disease is caused by the tick-borne spirochete, Borrelia burgdorferi. The spirochete produces over 100 membrane anchored lipoproteins. One lipoprotein, designated VlsE, changes its antigenic properties through DNA recombination, most likely to evade adaptive immune responses in the host. Here we demonstrate that VlsE is on the surface of the spirochete and exposed to the outside. Our hypothesis is that vlsE recombination is active in the host but not in the tick, which does not have an adaptive immune system. We characterized the number of vlsE alleles present in culture and at different stages of the Borrelia life cycle in the vector and host. The locus was stable in culture and in ticks, unlike in mice where many novel recombinants were readily observed. These results support the hypothesis that vlsE recombination is more frequent in the host than in ticks.