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Abstract
Abstract
In humans, genetic factors have long been suspected to contribute to the onset and outcome of tuberculosis. Such effects are difficult to identify owing to their complex inheritance, and to the confounding impact of environmental factors, notably pathogen-associated virulence determinants. Recently, forward genetic approaches in mouse models and in human populations have been used to elucidate a molecular basis for predisposition to mycobacterial diseases. The genetic dissection of host predisposition to infection with Mycobacterium bovis BCG and M. tuberculosis will help to define the key molecules involved in host antituberculous immunity and should provide new insights into this important infectious disease.