01800nas a2200277   4500000000100000008004100001653001900042653000800061653000900069653000900078653000900087653001200096653001000108100001100118700000900129700001200138700000900150700000900159700000900168700001100177700000900188700001000197245012300207520117800330022001401508       2016                            d10aSusceptibility10aSNP10aMITA10aMFN210aMAVS10aleprosy10aChina1 aWang D1 aLi G1 aZhang D1 aXu L1 aLi X1 aYu X1 aLong H1 aLi Y1 aYao Y00aGenetic variants of the MAVS, MITA and MFN2 genes are not associated with leprosy in Han Chinese from Southwest China.3 a<p>Leprosy is a chronic infectious disease caused by Mycobacterium leprae (M. leprae), which has massive genomic decay and dependence on host metabolism. Accumulating evidence showed a crucial role of mitochondria in metabolism and innate immunity. We hypothesized that the mitochondrial-related antimicrobial/antiviral immune genes MAVS (mitochondrial antiviral signaling protein), MITA (mediator of IRF3 activation) and MFN2 (mitofusin 2) would confer a risk to leprosy. In this study, we performed a case-control study to analyze 11 tag and/or non-synonymous SNPs of the MAVS, MITA and MFN2 genes in 527 leprosy patients and 583 healthy individuals, and directly sequenced the three genes in 80 leprosy patients with a family history from Yunnan, Southwest China. We found no association between these SNPs and leprosy (including its subtypes) based on the frequencies of alleles, genotypes and haplotypes between the cases and controls. There was also no enrichment of potential pathogenic variants of the three genes in leprosy patients. Our results suggested that genetic variants of the MAVS, MITA and MFN2 genes might not affect the susceptibility to leprosy.</p>
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