Human immunodeficiency virus and leprosy.

In summary, clinical leprosy does not appear to be more frequent in HIV-positive than in HIV-negative people in areas where both infections are endemic. There is no evidence that the paucibacillary to multibacillary distribution of patients is altered by HIV infection. There are reports that neuritis is more severe in co-infected people, and that reversal reactions (or, at least, new lesions) may be more frequent after therapy; but these reports are either poorly documented or poorly controlled. In several ways, this lack of expected leprosy is similar to the patterns of other low-virulent infections in HIV-positive patients in the tropics, such as MAC infection, Pneumocystis carinii and cytomegalovirus infection. Despite the presence of the agents in the environment and/or in the human host, they are infrequently encountered clinicopathologically. This is in marked contrast to their importance in industrialized countries. One explanation, as yet unproven, is that HIV-positive patients in the tropics do not live long enough in states of severe immunosuppression to develop these infections. Perhaps the same applies to M. leprae infection, whose incubation period can be measured in decades and whose clinical course may evolve over years, in contrast to the common reactivation of latent, virulent M. tuberculosis infection with its high morbidity. There may also be an analogy between leprosy and infection with Plasmodium falciparum, Strongyloides stercoralis and Entamoeba histolytica: these infections are controlled (or at least influenced) by cell-mediated immunity and, theoretically, should be more frequent in HIV-positive people than HIV-negatives. In fact they are not, and leprosy may be regarded as another 'missing infection in AIDS'.(ABSTRACT TRUNCATED AT 250 WORDS)