Abstract
BackgroundLeprosy is a chronic infectious disease caused by Mycobacterium leprae, an unculturable pathogen with an exceptionally eroded genome. The high level of inactivation of gene function in M. leprae, including many genes in its metabolic pathways, has led to a dependence on host energy production and nutritional products. We hypothesized that host cellular powerhouse - the mitochondria - may affect host susceptibility to M. leprae and the onset of clinical leprosy, and this may be reflected by mitochondrial DNA (mtDNA) background and mtDNA copy number.MethodsWe analyzed the mtDNA sequence variation of 534 leprosy patients and 850 matched controls from Yunnan Province and classified each subject by haplogroup. mtDNA copy number, taken to be proportional to mtDNA content, was measured in a subset of these subjects (296 patients and 231 controls) and 12 leprosy patients upon diagnosis.ResultsComparison of matrilineal components of the case and control populations revealed no significant difference. However, measurement of mtDNA copy number showed that lepromatous leprosy patients had a significantly higher mtDNA content than controls (P = 0.008). Past medical treatments had no effect on the alteration of mtDNA copy number.ConclusionsOur results suggested that mtDNA content, but not haplogroup, affects leprosy and this influence is limited to the clinical subtype of lepromatous leprosy.
Highlights
Leprosy is a chronic infectious disease caused by an obligate intracellular bacillus, Mycobacterium leprae
There was no significant difference in mitochondrial DNA (mtDNA) haplogroup frequency between the patients and controls (Table 1)
When the leprosy patients were classified into two groups (MB group [N = 288) and PB group [N = 256]) according to their clinical features, no haplogroup was found to be associated with leprosy subtype relative to controls (Table 1)
Summary
Leprosy is a chronic infectious disease caused by an obligate intracellular bacillus, Mycobacterium leprae. A comparison with M. tuberculosis, has shown that more than half of the functional genes are inactivated or have became pseudogenes in the M. leprae genome [3,4,5]. These inactivated genes, many of which are predicted to be actively involved in metabolic pathways, have resulted in M. leprae being an intracellular parasite. During the long evolutionary erosion of its genome, M. leprae has developed a dependence on host energy production and nutritional products and as a result the parasitic life and adaptation might have shaped host genetic susceptibility to leprosy [5,7,8]. We hypothesized that host cellular powerhouse - the mitochondria - may affect host susceptibility to M. leprae and the onset of clinical leprosy, and this may be reflected by mitochondrial DNA (mtDNA) background and mtDNA copy number
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