A study explores protective immunological mechanisms in a macaque model of coinfection with simian immunodeficiency virus (SIV) and Mycobacterium tuberculosis (Mtb), the bacterium that causes tuberculosis (TB). One in three people harbor latent Mtb, which can develop into active TB. Coinfection with human immunodeficiency virus (HIV) can speed the progression of latent TB to active TB, a process likely driven by a depletion of CD4+ T cells. To study the immunological regulation of latent TB infection by HIV, Deepak Kaushal and colleagues infected macaques with Mtb and SIV, mimicking Mtb and HIV coinfection in humans. In a majority of animals, Mtb replication rapidly reactivated and progressed to active TB, and pathologies associated with SIV increased. Despite the decrease in pulmonary CD4+ T cells in all coinfected macaques, one-third of the animals maintained TB latency. For this cohort, an increase in protective immune responses, mediated by CD8+ memory T-cell proliferation and increased B-cell responses, was associated with limited Mtb replication. According to the authors, the findings may provide insights into natural immunity to Mtb and could help guide the development of vaccines and immunotherapies for TB and HIV. - Read at PNAS.org
Article #16-11987: “CD4+ T-cell–independent mechanisms suppress reactivation of latent tuberculosis in a macaque model of HIV coinfection,” by Taylor W. Foreman et al.