Because leprosy is caused by an intracellular pathogen, production of circulating humoral antibodies (the immunoglobulins) is of little use in combatting the infection of cells and the multiplication of the organism in human tissues. Cell-mediated, or T-cell, immunity is thus the principal bodily means of combating leprosy. Individuals in whom the expression of cell-mediated immunity is compromised or poorly developed, such as pregnant women and children younger than 2 years of age, are at greater risk for both infection (when initially exposed) and progression of the disease unimpeded by the immune system. Others with intact cellular immunity can live almost 20 years before the first serious, debilitating consequences of infection occur. It is not known to what extent recurrent viral infection, which also challenges cellular immunity, may hasten the onset of clinical leprosy.

Genetic factors may further mediate the clinical expression of leprosy among those already infected, predisposing some individuals to a more or less rapid course of the disease, or perhaps influencing the appearance of severe, lepromatous leprosy rather than the milder tuberculoid form. Nevertheless, there are only a limited number of cases in which some clear genetic determinant of susceptibility can be differentiated from the socioeconomic factors mediating exposure to the agent.

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