Immunology of the lung in HIV infection: the pathophysiologic basis for the development of tuberculosis in the AIDS setting.
Active tuberculosis is now recognized as a frequent and serious complication of infection with the human immunodeficiency virus (HIV), the causative agent of AIDS. HIV mediated alteration in host defenses against mycobacteria contribute to the magnitude and severity of this problem. HIV can affect a variety of cellular mechanisms important in the restriction of mycobacterial growth. Qualitative and quantitative defects in T lymphocyte function result from direct HIV infection of cells expressing the CD4 epitope, and can severely limit the production of macrophage activating cytokines capable of inducing an anti-mycobacterial state in cells of monocyte lineage. In addition, macrophages themselves are susceptible to HIV infection, and have been shown to be defective with respect to a variety of host defense functions. Both T4 lymphopenia and HIV infected macrophages are present in the lower respiratory tract of HIV infected individuals, a circumstance which likely underlies the unique susceptibility of HIV infected to tuberculosis.
Rose
R M
RM
Section on Pulmonary and Critical Care Medicine, New England Deaconess Hospital, Boston, MA.
D000163:Acquired Immunodeficiency Syndrome / Q000097:blood / Q000150:complications / Q000276:immunology*; D000818:Animals; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008403:Mass Screening / Q000592:standards; D011817:Rabbits; D013601:T-Lymphocytes / Q000737:chemistry / Q000276:immunology; D014376:Tuberculosis / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control