Approximately 200,000 people contract leprosy every year, making it the second most common mycobacterial disease. This is surprising, because an effective treatment exists and Mycobacterium leprae (M. leprae), the organism that causes the disease, is only mildly infectious at best. Indeed, exposure to the slow-growing bacterium alone does not cause leprosy; disease risk depends on the interplay of several environmental and genetic factors.
In a recent Plos Neglected Tropical Diseases article, Vinicius Fava and his colleagues in Erwin Schurr’s laboratory at McGill University showcase how deep sequencing complements genome-wide association studies (GWAS) to pinpoint mutations that protected individuals from contracting leprosy.1 To do this, the researchers compared patient genomes with those of people who encountered the bacteria but did not fall ill. These risk factors shed light on the pathways that M. leprae hijacks to attack the body, enabling scientists to develop new ways to stop the bacterium’s spread.
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