Tuberculosis is the leading cause of death due to infectious diseases in the world today,
and it is increasing due to co-infection with HIV-1, the causative agent of AIDS. Here, we
examine the impact that HIV-1 infection has on persons with latent tuberculosis. Based on previous
work, we develop a mathematical model of an adaptive immune response in the lung which
considers relevant immune effectors such as macrophages, various sub-populations of T-cells, and
key cytokines to predict which mechanisms are important to HIV-1 infection induced reactivation
of tuberculosis. Our results indicate that persons latently infected with TB who are subsequently
co-infected with HIV-1 will suffer reactive TB. The mechanisms that contribute to this are essentially
related to a completely different cytokine environment at the onset of HIV-1 infection due
to the presence of Mycobacterium tuberculosis. Our analysis suggests that macrophages play an
important role during co-infection and decreases in macrophage counts are coupled to a decline in
CD4+ T-cells and increased viral loads. These mechanisms are also coupled to lower recruitment
of T-cells and macrophages, compromising protective immunity in the lung and eventually leading
to TB reactivation. These results point to potential targets for drug and vaccine therapies.