Interaction with human immunodeficiency virus type 1 modulates innate effector functions of human monocytes.
The effect of human immunodeficiency virus (HIV) type 1 on human mononuclear phagocyte effector functions in response to infection with bacteria of the Mycobacterium avium-intracellular complex (MAC) was investigated. The results showed that interaction of HIV-1 or its constituents with CD4 expressed in the monocyte membrane led to substantial impairment of monocyte capacity to restrict the intracellular growth of MAC. This was accompanied by substantially decreased production of tumor necrosis factor-alpha by HIV-1-exposed and MAC-infected monocytes. However, productive HIV-1 infection of monocytes was not required to induce the observed effects. These studies suggest that HIV-1 may interfere with innate mononuclear phagocyte function. This may be of physiologic importance in the late stages of AIDS, when an impaired T cell immunity can no longer provide proper immune-activating signals, and may help to explain the undue susceptibility to MAC infections in these patients.
Zerlauth
G
G
Immuno AG, University of Vienna, Austria.
Maier
E
E
Chehadeh
H
H
Zimmermann
K
K
Eibl
M M
MM
Mannhalter
J W
JW
D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D009000:Monocytes / Q000276:immunology* / Q000821:virology; D015269:Mycobacterium avium Complex / Q000254:growth & development; D015270:Mycobacterium avium-intracellulare Infection / Q000209:etiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D014409:Tumor Necrosis Factor-alpha