02008nas a2200373   4500000000100000008004100001260001300042653001500055653001000070653000900080653002500089653003800114653001300152653001100165653001200176653001100188653001600199653002600215653002700241100001400268700001200282700001700294700001400311700001600325700001500341700001200356700001100368245010700379856005100486300001100537490000700548520106500555022001401620       2004                            d  c2004 Sep10aAdolescent10aAdult10aAged10aCase-Control Studies10aGenetic Predisposition to Disease10agenotype10aHumans10aleprosy10aMalawi10aMiddle Aged10aPolymorphism, Genetic10aSequence Analysis, DNA1 aFitness J1 aFloyd S1 aWarndorff DK1 aSichali L1 aMwaungulu L1 aCrampin AC1 aFine PE1 aHill A00aLarge-scale candidate gene study of leprosy susceptibility in the Karonga district of northern Malawi.  uhttp://www.ajtmh.org/content/71/3/330.full.pdf  a330-400 v713 a<p>We present a large case-control candidate gene study of leprosy susceptibility. Thirty-eight polymorphic sites from 13 genes were investigated for their role in susceptibility to leprosy by comparing 270 cases with 452 controls in Karonga district, northern Malawi. Homozygotes for a silent T-->C change in codon 352 of the vitamin D receptor gene appeared to be at high risk (odds ratio [OR] = 4.3, 95% confidence interval [CI] = 1.6-11.4, P = 0.004), while homozygotes for the McCoy b blood group defining variant K1590E in exon 29 of the complement receptor 1 (formerly CD35) gene appeared to be protected (OR = 0.3, 95% CI = 0.1-0.8, P = 0.02). Borderline evidence for association with leprosy susceptibility was found for seven polymorphic sites in an additional six genes. Some of these apparent associations may be false-positive results from multiple comparisons, and several associations suggested by studies in other populations were not replicated here. These data provide evidence of inter-population heterogeneity in leprosy susceptibility.</p>  a0002-9637