Genetic Predisposition to Clinical Tuberculosis: Bridging the Gap between Simple and Complex Inheritance

Abstract

Tuberculosis, a chronic infectious disease caused by Mycobacterium tuberculosis, has reemerged as a leading public health problem. Approximately one-third of the world’s population is infected with M. tuberculosis, and a recent World Health Organization report estimated that, in 1998, there were 8 million new cases of clinical tuberculosis and 1.9 million deaths from the disease. Interestingly, not all individuals exposed to M. tuberculosis become infected. Moreover, progression toward clinical tuberculosis is far from an inevitable consequence of infection with M. tuberculosis, since only ∼10% of the vast number of infected individuals actually develop clinical disease (Bloom and Small 1998). Both M. tuberculosis infection and clinical tuberculosis result from complex interactions between the infectious agent, environmental factors, and the host.