Within host populations, individuals can vary in their susceptibility to infections and in the severity and progression of disease once infected. Though mediated through differences in behaviour, resistance or tolerance, variation in disease outcomes ultimately stems from genetic and environmental (including social) factors. Despite obvious implications for the evolutionary, ecological and epidemiological dynamics of disease traits, the relative importance of these factors has rarely been quantified in naturally infected wild animal hosts. Here, we use a long-term capture-mark-recapture study of group-living European badgers (Meles meles) to characterise genetic and environmental sources of variation in host infection status by Mycobacterium bovis, the causative agent of bovine tuberculosis (bTB). We find that genetic factors contribute to M. bovis infection status, whether measured over a lifetime or across repeated captures. In the latter case the heritability (h2 ) of infection status is close to zero in cubs and yearlings but increases in adulthood. Overall, environmental influences arising from a combination of social group membership (defined in time and space) and maternal effects appear to be more important than genetic factors. Thus, while genes do contribute to among-individual variation, they play a comparatively minor role, meaning that rapid evolution of host defences under parasite-mediated selection is unlikely (especially if selection is on young animals where h2 is lowest). Conversely, our results lend further support to the view that social and early-life environments are important drivers of the dynamics of bTB infection in badger populations specifically, and of disease traits in wild hosts more generally.