Abstract
Interferon (IFN)-γ, is not only a marker of TH1 CD4, CD8 and natural killer (NK) cells, it is also a critical antiviral mediator which is central to the elimination of viruses from the CNS. In this review, we describe IFN-γ, its receptor, signal transduction from receptor engagement, and antiviral downstream mediators. We demonstrate that although neurons are post-mitotic and non-renewing, they respond to IFN-γ in a fashion similar to peripheral fibroblasts or lymphocytes. We have illustrated this review with details about studies on the role(s) of IFN-γ in the pathogenesis of measles virus (MV), herpes simplex virus (HSV) type 1, and vesicular stomatitis virus (VSV) infections of the CNS. For VSV infection, IFN-γ signals through Jaks 1 and 2 and STAT1 to activate (interferon regulatory factor) IRF-1; although viral protein synthesis is inhibited, PKR is not a critical mediator in the antiviral response to VSV in murine neurons. In contrast, induction of nitric oxide synthase (NOS) type 1 and its production of nitric oxide is essential in the elimination of viruses from neurons.
Original language | English (US) |
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Pages (from-to) | 441-454 |
Number of pages | 14 |
Journal | Cytokine and Growth Factor Reviews |
Volume | 13 |
Issue number | 6 |
DOIs | |
State | Published - Dec 2002 |
Keywords
- Antiviral
- Interferon-γ
- Neuron
- Nitric oxide
- Virus
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Immunology and Allergy
- Immunology
- General Biochemistry, Genetics and Molecular Biology