Mycobacterium tuberculosis (MTB) and human immunodeficiency virus type 1 (H
IV-1) are virulent intracellular pathogens that enter and replicate within
macrophages, which represent their reservoire. Public health problems are g
reatly compounded when the two diseases co-exist, and this is the reason wh
y Acquired Immunodeficiency Syndrome (AIDS) and tuberculosis (TB) have been
termed "the cursed duet", given the synergistic effect they exert one each
other. With the depression of immunity caused by HIV-1 infection, latent M
TB infection is much more likely to progress to clinically significant dise
ase. On the other hand, TB results in activation of T cells and macrophages
that may harbor latent HIV. Here some data are reviewed that can contribut
e to clarify the mechanisms involved in the concurrent infection, given tha
t MTB infection has been shown to be able to: a) enhance HIV-1 replication
in macrophages, b) augment CC-CKR5 (CCR5) expression on macrophage membrane
, and, c) induce apoptosis in a portion of infected macrophages.