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The cause-and-effect relationship between severe infections and death suggests that microbial pathogens are evolutionary sculptors of the genome. However, the genetic component of susceptibility to infections in the general population is complex and heterogeneous and is modulated by environmental factors such as determinants of microbial virulence. Thus, it is a challenge to identify specific genetic effects in human populations. Availability of the human genome sequence, combined with knowledge of genetic variation, has facilitated the genomewide association study, a powerful approach to detecting genetic associations. In this issue of the Journal, Zhang and colleagues1 describe a genomewide association study of leprosy, . . .
Schurr et al. (Thu,) studied this question.
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