Abstract
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.
Original language | English (US) |
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Pages (from-to) | 43-54 |
Number of pages | 12 |
Journal | International Reviews of Immunology |
Volume | 8 |
Issue number | 1 |
DOIs | |
State | Published - 1992 |
Externally published | Yes |
Keywords
- Human immunodeficiency virus
- Interferon
- Macrophage
- Viral persistence
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology