Monocytes/macrophages in HIV infection and tuberculosis.
Mycobacterium tuberculosis (MTB) and human immunodeficiency virus type 1 (HIV-1) are virulent intracellular pathogens that enter and replicate within macrophages, which represent their reservoire. Public health problems are greatly compounded when the two diseases co-exist, and this is the reason why 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 MTB infection is much more likely to progress to clinically significant disease. 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 contribute to clarify the mechanisms involved in the concurrent infection, given that 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.
Sanduzzi
A
A
Monaldi Hospital, University of Naples Federico II, Italy.
Fraziano
M
M
Mariani
F
F
D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology*; D017209:Apoptosis; D015497:HIV-1 / Q000502:physiology; D006801:Humans; D008264:Macrophages / Q000382:microbiology / Q000502:physiology*; D009000:Monocytes / Q000382:microbiology / Q000502:physiology*; D019713:Receptors, CCR5 / Q000032:analysis; D014376:Tuberculosis / Q000276:immunology*; D014779:Virus Replication
D019713:Receptors, CCR5