To address the possibility that the lack of complementation (or attenuation of infection by WT B. burgdorferi) was a result of excess protein production due to higher copy number, we constructed a strain in which the ospC gene located on cp26 was replaced with the vlsE coding sequence, with the fusion between the ospC promoter at the start codon of the vlsE ORF (see Experimental procedures). The gene discussed is CYP26A1; the disease is infection.