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

Howard E. Gendelman, Donald R. Skillman, Monte S. Meltzer

Research output: Contribution to journalArticle

14 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)43-54
Number of pages12
JournalInternational Reviews of Immunology
Volume8
Issue number1
DOIs
StatePublished - Jan 1 1992

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Virus Diseases
Interferon-alpha
Macrophages
HIV
Monocytes
Virus Replication
Antiviral Agents
Immunity
Infection

Keywords

  • Human immunodeficiency virus
  • Interferon
  • Macrophage
  • Viral persistence

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

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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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