Moreover, allelic variation in OspC alters binding to extracellular matrix components, promotes joint invasion, and modulates joint colonization [81]; OspC has also been shown to bind to plasminogen [82,83], promote resistance in serum killing assays [84], and its role in causing infection can be, under certain circumstances, partially complemented by other surface lipoproteins [85,86]. This evidence concerns the gene PLG and infection.