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Bioscience Horizons Advance Access originally published online on April 9, 2009
Bioscience Horizons 2009 2(2):212-224; doi:10.1093/biohorizons/hzp014
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© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Viral evasion of interferon stimulated genes

John A.L. Short*

Institute of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK

* Corresponding author: John A. L. Short, 26 De Frene Road, Sydenham, London SE26 4AB, UK. Tel: +44 780 408 5575. Email: johnalshort{at}aol.com

Supervisor: Dr Andrew Macdonald, Institute of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK.


   Abstract

Viruses and their hosts since the dawn of time have been battling for supremacy. In recent years, the ‘Interferon Gateway’ encompassing interferon-alpha and -beta (IFN-{alpha}/β) expression, signalling and antiviral responses, has been uncovered. IFN-{alpha} are cytokines that co-ordinate the innate and adaptive immune responses to eliminate virus infections from the host. Interferon Stimulated Gene (ISG) products, such as protein kinase R, can prevent the translation of viral and cellular mRNAs to limit viral replication and can also initiate apoptosis if the cell is overwhelmed. In order to replicate, viruses have evolved viral evasion proteins that are able to target all aspects of the host response through a variety of sophisticated mechanisms. Viral evasion proteins can encode cellular domains to interact directly with ISGs and neutralize their function, hijack cellular pathways or degrade antiviral components. The high mutation rates associated with viral replication ensure that viruses will continue to adapt to our defences, but equally the viral evasion proteins are novel drug targets for eliminating or managing virus infections.

Key words: interferon, viral evasion, innate


Submitted on 2 December 2008; accepted on 11 February 2009


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