02102nas a2200253 4500000000100000008004100001100001800042700001300060700001500073700001300088700001200101700001300113700001000126700001200136700001100148700001300159700001400172245008500186856007800271300001300349490000700362520146500369022001401834 2016 d1 aGaschignard J1 aGrant AV1 aVan Thuc N1 aOrlova M1 aCobat A1 aHuong NT1 aBa NN1 aThai VH1 aAbel L1 aSchurr E1 aAlcaïs A00aPauci- and multibacillary leprosy: two distinct, genetically neglected diseases. uhttp://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0004345 ae00043450 v103 a

After sustained exposure to Mycobacterium leprae, only a subset of exposed individuals develops clinical leprosy. Moreover, leprosy patients show a wide spectrum of clinical manifestations that extend from the paucibacillary (PB) to the multibacillary (MB) form of the disease. This "polarization" of leprosy has long been a major focus of investigation for immunologists because of the different immune response in these two forms. But while leprosy per se has been shown to be under tight human genetic control, few epidemiological or genetic studies have focused on leprosy subtypes. Using PubMed, we collected available data in English on the epidemiology of leprosy polarization and the possible role of human genetics in its pathophysiology until September 2015. At the genetic level, we assembled a list of 28 genes from the literature that are associated with leprosy subtypes or implicated in the polarization process. Our bibliographical search revealed that improved study designs are needed to identify genes associated with leprosy polarization. Future investigations should not be restricted to a subanalysis of leprosy per se studies but should instead contrast MB to PB individuals. We show the latter approach to be the most powerful design for the identification of genetic polarization determinants. Finally, we bring to light the important resource represented by the nine-banded armadillo model, a unique animal model for leprosy.

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