01716nas a2200265   4500000000100000008004100001260001600042653001100058653001200069653001600081653002300097653002900120653002500149653003100174653001700205653001700222100001200239700001500251700001300266245007900279300001100358490000800369520105900377022001401436       1996                            d  c1996 Mar 2210aHumans10aleprosy10aMathematics10aModels, Biological10aMycobacterium Infections10aMycobacterium leprae10aMycobacterium tuberculosis10aTime Factors10aTuberculosis1 aAntia R1 aKoella J C1 aPerrot V00aModels of the within-host dynamics of persistent mycobacterial infections.  a257-630 v2633 a<p>We use mathematical models to investigate the within-host dynamics of mycobacterial infections. In particular, we investigate the mechanisms by which bacteria such as Mycobacterium tuberculosis and Mycobacterium leprae persist at low densities for extended periods, and attain high densities much later. We suggest that the persistence of bacteria in face of immune pressure may result from the bacteria having a very slow growth rate, or having a dormant stage. We show that whereas these mechanisms may lead to long-term persistence, this will be obtained at relatively low densities. We then suggest that the long-term persistence of bacteria may result in the loss of immunity because of the deletion of specific T-cells arriving from the thymus, and the exhaustion of the specific T-cells as these cells reach the Hayflick limit and die. This loss of immunity will allow the bacteria to attain a high density. We propose experiments capable of testing our models and discuss the implications of the models for the treatment of infected hosts.</p>  a0962-8452