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Evading the Interferon Response: Hepatitis C Virus and the Interferon-Induced Protein Kinase, PKR

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Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 242))

Abstract

What’s a cell to do when faced with the prospect of being invaded by an army of determined viruses? A complex, multi-pronged defense is in order, and luckily, just such a defense is available. The cellular interferon response represents a powerful and multi-faceted approach to dealing with everyday stresses that range from viral infection to keeping cellular growth under control. Mediated by a family of negative growth regulators, collectively referred to as interferons, the interferon response is indeed complex. After binding to specific cell surface receptors, interferons set in motion a number of signal transduction pathways that lead to the induction of gene expression (reviewed in FOSTER 1997; HAQUE and WILLIAMS 1998; MÜLLER et al. 1994; VILCEK and SEN 1996). Although the majority of in-terferon-induced gene products have yet to be characterized, several have demonstrated antiviral properties. These include RNase L, 2′–5′ oligoadenylate synthetase, the Mx proteins, and the double-stranded (ds)RNA-activated protein kinase, PKR. Together, these proteins are capable of disrupting viral gene expression at multiple levels, including viral mRNA stability, transcription, and translation. Of course, viruses are not without weapons of their own, and many are capable of putting up a good fight, and even winning, in the face of such an arsenal. In this review, we will focus our attention on one particular component of the cellular antiviral response, the protein kinase known as PKR. PKR is one of the better characterized interferon-induced gene products and is critical component of the antiviral response.

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Korth, M.J., Katze, M.G. (2000). Evading the Interferon Response: Hepatitis C Virus and the Interferon-Induced Protein Kinase, PKR. In: Hagedorn, C.H., Rice, C.M. (eds) The Hepatitis C Viruses. Current Topics in Microbiology and Immunology, vol 242. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-59605-6_10

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