These factors, together with the long human co-existence with M. leprae[34] and intense social stigma associated with the disease [35], suggest that leprosy may have contributed to the present global distribution of human TLR1. Other infectious diseases especially tuberculosis could have also contributed, given the overlapping antigenic repertoire and immunogenicity of mycobacterial species, despite a lack of association in a Gambian case-control population due to low allele frequency (Table S13). This evidence concerns the gene TLR1 and leprosy.