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Interferon alpha (IFN)-macrophage interactions in human immunodeficiency virus (HIV) infection: role of IFN in the tempo and progression of HIV disease.

Authors
  • Gendelman, H E
  • Skillman, D R
  • Meltzer, M S
Type
Published Article
Journal
International reviews of immunology
Publication Date
Jan 01, 1992
Volume
8
Issue
1
Pages
43–54
Identifiers
PMID: 1573319
Source
Medline
License
Unknown

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.

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