Unlike other opportunistic infections associated with human immunodeficiency virus (HIV) type 1, tuberculosis (TB) occurs throughout the course of HIV-1 infection, and, as a chronic infection, its impact on viral activity is sustained. In dually infected subjects, HIV-1 load and heterogeneity are increased both locally and systemically during active TB. Studies over the past decade have indicated that Mycobacterium tuberculosis (MTB) infection supports HIV-1 replication and dissemination through the dysregulation of host cytokines, chemokines, and their receptors. Furthermore, concentrations of HIV-1 inhibitory chemokines are limited during TB and at sites of MTB infection. Cumulatively, these data indicate that TB provides a milieu of continuous cellular activation and irregularities in cytokine and chemokine circuits that are permissive of viral replication and expansion in situ. I address new research that has identified the basis for the augmentation of HIV-1 replication during TB and discuss potential immunotherapies to contain viral expansion during TB.