Interferon alpha (IFN)-macrophage interactions in human immunodeficiency virus (HIV) infection: role of IFN in the tempo and progression of HIV disease.
Components of the host immune response that constrain virus replication and affect long-lasting antiviral immunity following HIV infection are incompletely defined. IFNs are critical participants in host antiviral processes. While IFN induces significant anti-retroviral activities, they also serve as harbingers for poor clinical outcomes. Moreover, monocytes, a major cellular source of IFN and HIV in man, are poor producer cells for IFN following HIV infection. Indeed, HIV infection of monocytes results in a diminished production and induction of IFN. IFN is only produced during cell to cell contact between HIV-infected cells and uninfected PBMC. Analysis of the biologic activity of HIV-induced IFN(s) shows that it poorly restricts HIV replication. Thus, the role of IFN in HIV disease is complex and seemingly paradoxical. The diminished capacity of HIV-infected monocytes to produce IFN and the production of defective IFNs likely reflect specific viral adaptive mechanisms for persistent infection.
Gendelman
H E
HE
Department of Cellular Immunology, Walter Reed Army Institute of Research, Rockville, Maryland.
Skillman
D R
DR
Meltzer
M S
MS
D006678:HIV / Q000254:growth & development; D015658:HIV Infections / Q000276:immunology*; D006801:Humans; D016898:Interferon-alpha / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D009000:Monocytes / Q000382:microbiology; D014779:Virus Replication
D016898:Interferon-alpha