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Genetics of Leprosy

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Leprosy

Abstract

Clinical and epidemiological observations suggest that only a small proportion of the population exposed to Mycobacterium leprae develops the disease. The near-clonal characteristic of M. leprae and the wide range of leprosy clinical phenotypes strongly suggest that most of the observed variability, including susceptibility to disease per se, strongly depends on the genetic background of the host. Today, there is a large body of evidence confirming this hypothesis; for example, several complex segregation analyses have detected a strong genetic component controlling leprosy susceptibility; other studies have reported a strong familial component for the disease, as well as increased concordance of leprosy in monozygotic versus dizygotic twins. The genetic hypothesis has been further strengthened by studies linking or associating leprosy susceptibility to several candidate genes, for example, human leukocyte antigen (HLA) class I and II variants that seem to be independently modified by TNFA, LTA, and TAP polymorphisms. In addition, non-HLA genes have been implicated in leprosy susceptibility, such as PARK2/PACRG, NOD2, NRAMP1, MRC1, and IL10. In this chapter, we summarize the latest advances in the field of host genetic susceptibility to leprosy phenotypes.

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Correspondence to Marcelo Távora Mira .

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© 2012 Springer-Verlag Italia

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Fava, V.M., Mira, M.T. (2012). Genetics of Leprosy. In: Nunzi, E., Massone, C. (eds) Leprosy. Springer, Milano. https://doi.org/10.1007/978-88-470-2376-5_3

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  • DOI: https://doi.org/10.1007/978-88-470-2376-5_3

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  • Publisher Name: Springer, Milano

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