Abstract
Summary. Tuberculosis is re-emerging as a leading public health problem worldwide, largely due to the lack of a fully protective vaccine, the acquired immunodeficiency associated with HIV-co-infection and the increasing number of drug-resistant mycobacteria. There is substantial epidemiological evidence that the host genetic make-up affects the development of clinical tuberculosis in humans. Here we review population-based and patient-based molecular studies that have implicated various genes in polygenic and monogenic susceptibility to mycobacterial disease. We further discuss the possibility of a continuous spectrum between these two poles of tuberculosis genetics.
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